sulforaphane and Inflammation studies

sulforaphane: from Cardaria draba L.
sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.

Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.

Research Excerpts

Excerpt	Relevance	Reference
"Sulforaphane can reduce sepsis-induced inflammatory responses and enhance myogenic differentiation by regulating the TLR4 and NLRP3 inflammasome pathways."	8.31	Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. ( Gan, L; Liu, M; Teng, Z; Wang, M; Wu, X; Xu, W; Zhang, Y, 2023)
" This study aimed to investigate the protective potential of sulforaphane (SF), nuclear factor E2 related factor (Nrf-2) activator, against CPZ-induced cardiotoxicity and hepatotoxicity."	8.31	Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity. ( Ibrahim Fouad, G, 2023)
" Activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-pathway, which is important in controlling inflammation and oxidative stress that occur during aging, can be triggered by sulforaphane (SFN), an isothiocyanate found in plants from the Brassicaceae family."	8.02	Dietary supplementation with sulforaphane ameliorates skin aging through activation of the Keap1-Nrf2 pathway. ( Alves, I; Awasthi, S; Bose, C; Børsheim, E; Carvalho, E; Dalgaard, LT; Leal, EC; Palade, PT; Petkovic, M; Singh, P; Singh, SP, 2021)
"BACKGROUND The aim of this study was to investigate the effects of sulforaphane (SFN), a natural isothiocyanate compound, in a rabbit ascending aortic cerclage model of chronic heart failure (CHF)."	7.88	Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure. ( Chen, D; Dong, H; Lu, H; Ma, T; Wu, G; Wu, W; Zhang, Q; Zhu, D, 2018)
"The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and inflammation in rats liver with toxic hepatitis induced by acetaminophene."	7.85	The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene. ( Aktas, MS; Dokumacioglu, A; Dokumacioglu, E; Hanedan, B; Iskender, H; Musmul, A; Sen, TM, 2017)
" Sulforaphane could be a new therapeutic approach to improve cognitive and motor function in hyperammonemia, hepatic encephalopathy, and other pathologies associated with neuroinflammation by promoting microglia differentiation from M1 to M2."	7.83	Neuroinflammation increases GABAergic tone and impairs cognitive and motor function in hyperammonemia by increasing GAT-3 membrane expression. Reversal by sulforaphane by promoting M2 polarization of microglia. ( Agusti, A; Balzano, T; Cabrera-Pastor, A; Felipo, V; Gonzalez-Usano, A; Hernandez-Rabaza, V; Llansola, M; Taoro-Gonzalez, L, 2016)
"In our study, we investigate whether the oxyhemoglobin (OxyHb) can induce the activation of the Nrf2-ARE pathway in vascular smooth muscle cells (VSMCs), and evaluate the modulatory effects of sulforaphane (SUL) on OxyHb-induced inflammation in VSMCs."	7.79	Sulforaphane enhances the activity of the Nrf2-ARE pathway and attenuates inflammation in OxyHb-induced rat vascular smooth muscle cells. ( Lu, XJ; Zhao, XD; Zhou, YT, 2013)
"Chronic inflammation and selenium deficiency are considered as risk factors for colon cancer."	7.78	Glutathione peroxidase-2 and selenium decreased inflammation and tumors in a mouse model of inflammation-associated carcinogenesis whereas sulforaphane effects differed with selenium supply. ( Banning, A; Brauer, MN; Brigelius-Flohé, R; Chu, FF; Esworthy, RS; Florian, S; Iori, R; Kipp, AP; Krehl, S; Loewinger, M; Wessjohann, LA, 2012)
"Sulforaphane was administered at a daily dose of 50 μmol (≤45 kg) or 100 μmol (>45 kg)."	6.94	Sulforaphane as an adjunctive treatment for irritability in children with autism spectrum disorder: A randomized, double-blind, placebo-controlled clinical trial. ( Akhondzadeh, S; Amirimoghaddam-Yazdi, Z; Moghaddam, HS; Mohammadi, MR; Momtazmanesh, S, 2020)
"Sulforaphane (SFN) is a natural isothiocyanate extracted from cruciferous vegetables with promising anti-inflammatory and anti-oxidative activities."	5.91	Sulforaphane alleviated vascular remodeling in hypoxic pulmonary hypertension via inhibiting inflammation and oxidative stress. ( Cheng, K; Gong, M; Ji, Y; Li, J; Liu, L; Liu, Q; Pan, J; Pei, Y; Sun, J; Tang, Q; Wang, D; Wang, R; Wu, N; Yuan, Y; Zhang, C; Zheng, X, 2023)
"Sulforaphane (SFN) has a strong anti-inflammatory ability and a certain protective effect on intestinal diseases."	5.91	The Protective Effect of Sulforaphane on ER-induced Apoptosis and Inflammation in Necrotizing Enterocolitis Mice. ( Bao, Z; Mi, Y; Wang, X; Xiong, X, 2023)
"Psoriasis is a chronic inflammatory skin disease that affects millions of people worldwide."	5.91	Sulforaphane alleviates psoriasis by enhancing antioxidant defense through KEAP1-NRF2 Pathway activation and attenuating inflammatory signaling. ( Gu, C; Huang, Z; Li, L; Lian, P; Lu, R; Lu, Y; Ma, C; Peng, Z; Pu, W; Ruan, B; Su, Z; Wang, H; Wang, W; Wazir, J; Wei, L; Zong, Y, 2023)
"Sulforaphane was reported to ameliorate inflammatory responses."	5.72	Attenuation of experimentally induced atopic dermatitis in mice by sulforaphane: effect on inflammation and apoptosis. ( Alyoussef, A, 2022)
"Inflammation is a prominent feature of COPD and represents an important target for treatment."	5.62	Sulforaphane suppresses lipopolysaccharide- and Pam3CysSerLys4-mediated inflammation in chronic obstructive pulmonary disease via toll-like receptors. ( Bao, H; Liu, X; Zeng, X, 2021)
"Neuroinflammation is a potent pathological process of various neurodegenerative diseases."	5.56	Sulforaphane mitigates LPS-induced neuroinflammation through modulation of Cezanne/NF-κB signalling. ( Chen, LW; Chen, Q; Wang, J; Wang, ZC; Yu, LS, 2020)
"Treatment with sulforaphane restored animals' body weight, reduced blood glucose, glycated hemoglobin, and increased insulin levels."	5.48	Extracellular Matrix Remodeling and Modulation of Inflammation and Oxidative Stress by Sulforaphane in Experimental Diabetic Peripheral Neuropathy. ( Abdelkader, NF; El Awdan, SA; El-Shabrawy, OA; Moustafa, PE; Zaki, HF, 2018)
"Sulforaphane (SFN) is a natural compound that has been suggested as an antioxidant."	5.48	Sulforaphane Modulates Joint Inflammation in a Murine Model of Complete Freund's Adjuvant-Induced Mono-Arthritis. ( Abreu-Silva, AL; da Penha, TA; de Aquino, AF; de Sá, JC; de Souza, BGGF; Fialho Sousa, NC; França Muniz, T; Grisotto, MAG; Nascimento da Silva, LC; Neuza da Silva Nina, L; Silva E Silva, C; Silva Rodrigues, JF; Soares Fernandes, E, 2018)
"Inflammation is widely distributed in patients with Duchenne muscular dystrophy and ultimately leads to progressive deterioration of muscle function with chronic muscle damage, oxidative stress, and reduced oxidative capacity."	5.42	Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling Pathway. ( Li, DJ; Li, SJ; Sun, CC; Wang, L; Xi, YY; Xue, RL; Yang, CL; Zhao, QL, 2015)
"Sulforaphane (SFN) is an organosulfur compound present in vegetables and has potent anti-oxidant and anti-inflammatory activities."	5.39	Sulforaphane ameliorates the development of experimental autoimmune encephalomyelitis by antagonizing oxidative stress and Th17-related inflammation in mice. ( Cui, W; Ge, XL; Guo, L; Li, B; Li, R; Liu, J; Liu, Q; Song, XJ; Wang, Y; Xie, XH; Zhang, J, 2013)
"Sulforaphane (SFN) is a natural isothiocyanate that is present in cruciferous vegetables such as broccoli and cabbage."	5.35	Sulforaphane suppressed LPS-induced inflammation in mouse peritoneal macrophages through Nrf2 dependent pathway. ( Khor, TO; Kong, AN; Lin, W; Wang, H; Wu, RT; Wu, T, 2008)
"Sulforaphane can reduce sepsis-induced inflammatory responses and enhance myogenic differentiation by regulating the TLR4 and NLRP3 inflammasome pathways."	4.31	Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. ( Gan, L; Liu, M; Teng, Z; Wang, M; Wu, X; Xu, W; Zhang, Y, 2023)
" This study aimed to investigate the protective potential of sulforaphane (SF), nuclear factor E2 related factor (Nrf-2) activator, against CPZ-induced cardiotoxicity and hepatotoxicity."	4.31	Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity. ( Ibrahim Fouad, G, 2023)
"Chronic low-grade systemic inflammation (SI), including activation of the NLRP3 inflammasome, is a feature of obesity, associated with increased circulating saturated fatty acids, such as palmitic acid (PA), and bacterial endotoxin lipopolysaccharide (LPS)."	4.12	Sulforaphane reduces pro-inflammatory response to palmitic acid in monocytes and adipose tissue macrophages. ( Baines, KJ; Berthon, BS; Eslick, S; Gately, M; Guilleminault, L; Karihaloo, C; Williams, EJ; Wood, LG; Wright, T, 2022)
" Inflammation and oxidative stress are the primary factors underlying angiotensin II (Ang II)-induced aortic damage."	4.12	Essential role of Nrf2 in sulforaphane-induced protection against angiotensin II-induced aortic injury. ( Jiang, X; Liu, W; Meng, L; Tian, Y; Wang, H; Xin, Y; Zhang, Q, 2022)
" Activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-pathway, which is important in controlling inflammation and oxidative stress that occur during aging, can be triggered by sulforaphane (SFN), an isothiocyanate found in plants from the Brassicaceae family."	4.02	Dietary supplementation with sulforaphane ameliorates skin aging through activation of the Keap1-Nrf2 pathway. ( Alves, I; Awasthi, S; Bose, C; Børsheim, E; Carvalho, E; Dalgaard, LT; Leal, EC; Palade, PT; Petkovic, M; Singh, P; Singh, SP, 2021)
" The aim of this study was to investigate the hypothesis that polyacetylene falcarinol (FA) reduces intestinal inflammation and examine its similarity of effect to isothiocyanate R-sulforaphane during the late phase of acute inflammation."	3.96	Dietary polyacetylene falcarinol upregulated intestinal heme oxygenase-1 and modified plasma cytokine profile in late phase lipopolysaccharide-induced acute inflammation in CB57BL/6 mice. ( Bakovic, M; Stefanson, A, 2020)
"BACKGROUND The aim of this study was to investigate the effects of sulforaphane (SFN), a natural isothiocyanate compound, in a rabbit ascending aortic cerclage model of chronic heart failure (CHF)."	3.88	Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure. ( Chen, D; Dong, H; Lu, H; Ma, T; Wu, G; Wu, W; Zhang, Q; Zhu, D, 2018)
"The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and inflammation in rats liver with toxic hepatitis induced by acetaminophene."	3.85	The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene. ( Aktas, MS; Dokumacioglu, A; Dokumacioglu, E; Hanedan, B; Iskender, H; Musmul, A; Sen, TM, 2017)
" Sulforaphane could be a new therapeutic approach to improve cognitive and motor function in hyperammonemia, hepatic encephalopathy, and other pathologies associated with neuroinflammation by promoting microglia differentiation from M1 to M2."	3.83	Neuroinflammation increases GABAergic tone and impairs cognitive and motor function in hyperammonemia by increasing GAT-3 membrane expression. Reversal by sulforaphane by promoting M2 polarization of microglia. ( Agusti, A; Balzano, T; Cabrera-Pastor, A; Felipo, V; Gonzalez-Usano, A; Hernandez-Rabaza, V; Llansola, M; Taoro-Gonzalez, L, 2016)
"Okadaic acid (OKA) causes memory impairment and attenuates nuclear factor erythroid 2-related factor 2 (Nrf2) along with oxidative stress and neuroinflammation in rats."	3.83	Sulforaphane Ameliorates Okadaic Acid-Induced Memory Impairment in Rats by Activating the Nrf2/HO-1 Antioxidant Pathway. ( Dwivedi, S; Hanif, K; Nath, C; Rajasekar, N; Shukla, R, 2016)
" We investigate whether sulforaphane (SF), an isothiocyanate (ITC) obtained from broccoli, could suppress LPS-induced transcription and subsequent pro-inflammatory cytokine secretion at a physiologically relevant concentration using in vitro models of chronic inflammation."	3.80	Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. ( Al-Bakheit, A; Folkard, DL; Melchini, A; Mithen, RF; Mulholland, F; Saha, S; Traka, MH; Watson, A, 2014)
"In our study, we investigate whether the oxyhemoglobin (OxyHb) can induce the activation of the Nrf2-ARE pathway in vascular smooth muscle cells (VSMCs), and evaluate the modulatory effects of sulforaphane (SUL) on OxyHb-induced inflammation in VSMCs."	3.79	Sulforaphane enhances the activity of the Nrf2-ARE pathway and attenuates inflammation in OxyHb-induced rat vascular smooth muscle cells. ( Lu, XJ; Zhao, XD; Zhou, YT, 2013)
"Chronic inflammation and selenium deficiency are considered as risk factors for colon cancer."	3.78	Glutathione peroxidase-2 and selenium decreased inflammation and tumors in a mouse model of inflammation-associated carcinogenesis whereas sulforaphane effects differed with selenium supply. ( Banning, A; Brauer, MN; Brigelius-Flohé, R; Chu, FF; Esworthy, RS; Florian, S; Iori, R; Kipp, AP; Krehl, S; Loewinger, M; Wessjohann, LA, 2012)
"Sulforaphane was administered at a daily dose of 50 μmol (≤45 kg) or 100 μmol (>45 kg)."	2.94	Sulforaphane as an adjunctive treatment for irritability in children with autism spectrum disorder: A randomized, double-blind, placebo-controlled clinical trial. ( Akhondzadeh, S; Amirimoghaddam-Yazdi, Z; Moghaddam, HS; Mohammadi, MR; Momtazmanesh, S, 2020)
"Patients with chronic obstructive pulmonary disease (COPD) have high oxidative stress associated with the severity of the disease."	2.90	Compartmentalization of anti-oxidant and anti-inflammatory gene expression in current and former smokers with COPD. ( Berenson, CS; Biswal, S; Burke, A; Criner, GJ; Fahey, JW; Holbrook, JT; Jacobs, MR; Sethi, S; Sidhaye, VK; Sudini, KR; Thimmulappa, R; Wise, RA, 2019)
"Chronic inflammation has a significant impact on the quality of life of affected individuals with an increased risk of developing other chronic inflammatory diseases."	2.66	The potential use of l-sulforaphane for the treatment of chronic inflammatory diseases: A review of the clinical evidence. ( Karagiannis, TC; Licciardi, PV; Mazarakis, N; Snibson, K, 2020)
"Sulforaphane (SFN) has a strong anti-inflammatory ability and a certain protective effect on intestinal diseases."	1.91	The Protective Effect of Sulforaphane on ER-induced Apoptosis and Inflammation in Necrotizing Enterocolitis Mice. ( Bao, Z; Mi, Y; Wang, X; Xiong, X, 2023)
"Sulforaphane (SFN) is a natural isothiocyanate extracted from cruciferous vegetables with promising anti-inflammatory and anti-oxidative activities."	1.91	Sulforaphane alleviated vascular remodeling in hypoxic pulmonary hypertension via inhibiting inflammation and oxidative stress. ( Cheng, K; Gong, M; Ji, Y; Li, J; Liu, L; Liu, Q; Pan, J; Pei, Y; Sun, J; Tang, Q; Wang, D; Wang, R; Wu, N; Yuan, Y; Zhang, C; Zheng, X, 2023)
"Sulforaphane (SFN) is an isothiocyanate of vegetable origin with potent antioxidant and immunomodulatory properties."	1.91	Sulforaphane Reduces the Chronic Inflammatory Immune Response of Human Dendritic Cells. ( Alba, G; Brasal-Prieto, M; Cejudo-Guillen, M; Dakhaoui, H; Fernandez-Prades, L; Granados, B; Lopez-Enriquez, S; Martin, V; Montserrat-de la Paz, S; Palomares, F; Santa-Maria, C; Sobrino, F, 2023)
"Psoriasis is a chronic inflammatory skin disease that affects millions of people worldwide."	1.91	Sulforaphane alleviates psoriasis by enhancing antioxidant defense through KEAP1-NRF2 Pathway activation and attenuating inflammatory signaling. ( Gu, C; Huang, Z; Li, L; Lian, P; Lu, R; Lu, Y; Ma, C; Peng, Z; Pu, W; Ruan, B; Su, Z; Wang, H; Wang, W; Wazir, J; Wei, L; Zong, Y, 2023)
"Sulforaphane was reported to ameliorate inflammatory responses."	1.72	Attenuation of experimentally induced atopic dermatitis in mice by sulforaphane: effect on inflammation and apoptosis. ( Alyoussef, A, 2022)
"Inflammation is a prominent feature of COPD and represents an important target for treatment."	1.62	Sulforaphane suppresses lipopolysaccharide- and Pam3CysSerLys4-mediated inflammation in chronic obstructive pulmonary disease via toll-like receptors. ( Bao, H; Liu, X; Zeng, X, 2021)
"Acrylamide is a well characterized neurotoxicant known to cause neuropathy and encephalopathy in humans and experimental animals."	1.62	Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice. ( Davuljigari, CB; Ekuban, FA; Fergany, AAM; Ichihara, G; Morikawa, K; Zong, C, 2021)
"Sulforaphane treatment reduced the arthritis score and the severity of histologic inflammation in CIA mice."	1.62	The anti-arthritis effect of sulforaphane, an activator of Nrf2, is associated with inhibition of both B cell differentiation and the production of inflammatory cytokines. ( Cho, ML; Jhun, J; Jung, K; Kim, SY; Kwon, JY; Min, JK; Moon, SJ; Ryu, J, 2021)
"Neuroinflammation is a potent pathological process of various neurodegenerative diseases."	1.56	Sulforaphane mitigates LPS-induced neuroinflammation through modulation of Cezanne/NF-κB signalling. ( Chen, LW; Chen, Q; Wang, J; Wang, ZC; Yu, LS, 2020)
"Sulforaphane (SFN) prevents diabetic nephropathy (DN) in type 2 diabetes (T2D) by up-regulating nuclear factor (erythroid-derived 2)-like 2 (Nrf2)."	1.56	Sulforaphane prevents type 2 diabetes-induced nephropathy via AMPK-mediated activation of lipid metabolic pathways and Nrf2 antioxidative function. ( Cai, L; Guo, H; Li, J; Li, Z; Ma, T; Miao, L; Zhang, Z; Zhou, S, 2020)
"Pretreatment with sulforaphane prevented OD-induced inflammation and AHR while increasing the uptake of OD in bronchial epithelial cells."	1.51	Organic dust, causing both oxidative stress and Nrf2 activation, is phagocytized by bronchial epithelial cells. ( Adner, M; Chen, M; Farahnak, S; Larsson, K; Martin, JG; McGovern, T, 2019)
"Treatment with sulforaphane restored animals' body weight, reduced blood glucose, glycated hemoglobin, and increased insulin levels."	1.48	Extracellular Matrix Remodeling and Modulation of Inflammation and Oxidative Stress by Sulforaphane in Experimental Diabetic Peripheral Neuropathy. ( Abdelkader, NF; El Awdan, SA; El-Shabrawy, OA; Moustafa, PE; Zaki, HF, 2018)
"Sulforaphane (SFN) is a natural compound that has been suggested as an antioxidant."	1.48	Sulforaphane Modulates Joint Inflammation in a Murine Model of Complete Freund's Adjuvant-Induced Mono-Arthritis. ( Abreu-Silva, AL; da Penha, TA; de Aquino, AF; de Sá, JC; de Souza, BGGF; Fialho Sousa, NC; França Muniz, T; Grisotto, MAG; Nascimento da Silva, LC; Neuza da Silva Nina, L; Silva E Silva, C; Silva Rodrigues, JF; Soares Fernandes, E, 2018)
"Sepsis is often characterized by an acute brain inflammation and dysfunction, which is associated with increased morbidity and mortality worldwide."	1.43	Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways. ( Alexander, JS; Becker, F; Evans, PC; Gavins, FNE; Gillespie, S; Holloway, PM; Nguyen, V; Vital, SA, 2016)
"Inflammation is widely distributed in patients with Duchenne muscular dystrophy and ultimately leads to progressive deterioration of muscle function with chronic muscle damage, oxidative stress, and reduced oxidative capacity."	1.42	Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling Pathway. ( Li, DJ; Li, SJ; Sun, CC; Wang, L; Xi, YY; Xue, RL; Yang, CL; Zhao, QL, 2015)
"Sulforaphane (SFN) is an organosulfur compound present in vegetables and has potent anti-oxidant and anti-inflammatory activities."	1.39	Sulforaphane ameliorates the development of experimental autoimmune encephalomyelitis by antagonizing oxidative stress and Th17-related inflammation in mice. ( Cui, W; Ge, XL; Guo, L; Li, B; Li, R; Liu, J; Liu, Q; Song, XJ; Wang, Y; Xie, XH; Zhang, J, 2013)
"Sulforaphane (SFN) is a natural isothiocyanate that is present in cruciferous vegetables such as broccoli and cabbage."	1.35	Sulforaphane suppressed LPS-induced inflammation in mouse peritoneal macrophages through Nrf2 dependent pathway. ( Khor, TO; Kong, AN; Lin, W; Wang, H; Wu, RT; Wu, T, 2008)

Research

Studies (82)

Authors

Clinical Trials (4)

Trial Overview

Trial Outcomes

Change From Baseline in Bronchial Epithelial Cell Expression of AKR1C1 at 4 Weeks

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	1 (1.22)	29.6817
2010's	45 (54.88)	24.3611
2020's	36 (43.90)	2.80

Authors	Studies
Li, W	1
Zheng, S	1
Higgins, M	1
Morra, RP	1
Mendis, AT	1
Chien, CW	1
Ojima, I	1
Mierke, DF	1
Dinkova-Kostova, AT	2
Honda, T	1
Gu, X	1
Chen, J	2
Zhang, Y	5
Guan, M	1
Li, X	1
Zhou, Q	1
Song, Q	1
Qiu, J	1
Alyoussef, A	1
Yepes-Molina, L	1
Pérez-Jiménez, MI	1
Martínez-Esparza, M	1
Teruel, JA	1
Ruiz-Alcaraz, AJ	1
García-Peñarrubia, P	1
Carvajal, M	1
Williams, EJ	1
Guilleminault, L	1
Berthon, BS	1
Eslick, S	1
Wright, T	1
Karihaloo, C	1
Gately, M	1
Baines, KJ	1
Wood, LG	1
Çakır, I	1
Lining Pan, P	1
Hadley, CK	1
El-Gamal, A	1
Fadel, A	1
Elsayegh, D	1
Mohamed, O	1
Rizk, NM	1
Ghamari-Langroudi, M	1
Banerjee, N	2
Wang, H	5
Wang, G	2
Boor, PJ	1
Khan, MF	2
Wang, X	1
Mi, Y	1
Xiong, X	1
Bao, Z	1
Tian, Y	1
Zhang, Q	2
Liu, W	1
Meng, L	1
Jiang, X	1
Xin, Y	1
Pan, J	1
Wang, R	1
Pei, Y	1
Wang, D	2
Wu, N	1
Ji, Y	1
Tang, Q	1
Liu, L	1
Cheng, K	1
Liu, Q	3
Sun, J	2
Gong, M	1
Zheng, X	1
Li, J	2
Zhang, C	2
Yuan, Y	1
Wang, M	3
Liu, M	3
Xu, W	3
Teng, Z	3
Wu, X	4
Gan, L	3
Ibrahim Fouad, G	1
Xu, Y	1
Huang, X	1
Huangfu, B	1
Hu, Y	1
Xu, J	1
Gao, R	1
Huang, K	1
He, X	1
Fernandez-Prades, L	1
Brasal-Prieto, M	1
Alba, G	1
Martin, V	1
Montserrat-de la Paz, S	1
Cejudo-Guillen, M	1
Santa-Maria, C	1
Dakhaoui, H	1
Granados, B	1
Sobrino, F	1
Palomares, F	1
Lopez-Enriquez, S	1
Ma, J	1
Wang, B	1
Pu, C	1
Chang, K	1
Cheng, Y	1
Sun, R	1
Qi, Q	1
Xu, R	1
Ma, C	1
Gu, C	1
Lian, P	1
Wazir, J	1
Lu, R	1
Ruan, B	1
Wei, L	1
Li, L	1
Pu, W	1
Peng, Z	1
Wang, W	2
Zong, Y	1
Huang, Z	1
Lu, Y	1
Su, Z	1
Sidhaye, VK	1
Holbrook, JT	1
Burke, A	1
Sudini, KR	1
Sethi, S	1
Criner, GJ	1
Fahey, JW	2
Berenson, CS	1
Jacobs, MR	1
Thimmulappa, R	1
Wise, RA	1
Biswal, S	1
Liu, H	2
Zimmerman, AW	1
Singh, K	1
Connors, SL	1
Diggins, E	1
Stephenson, KK	1
Deramaudt, TB	2
Ali, M	2
Vinit, S	2
Bonay, M	2
Momtazmanesh, S	1
Amirimoghaddam-Yazdi, Z	1
Moghaddam, HS	1
Mohammadi, MR	1
Akhondzadeh, S	1
Hashimoto, K	2
Olcum, M	1
Tastan, B	2
Ercan, I	1
Eltutan, IB	1
Genc, S	2
Vanhee, V	1
Liu, J	3
Chandaka, GK	1
Zhang, R	1
Parfenova, H	1
Stefanson, A	1
Bakovic, M	1
Li, Z	1
Guo, H	1
Ma, T	2
Zhou, S	1
Zhang, Z	2
Miao, L	2
Cai, L	2
Wang, ZC	1
Chen, Q	1
Wang, J	1
Yu, LS	1
Chen, LW	1
Zinovkin, RA	1
Grebenchikov, OA	1
Abouzed, TK	1
Beltagy, ER	1
Kahilo, KA	1
Ibrahim, WM	1
Latronico, T	1
Larocca, M	1
Milella, S	1
Fasano, A	1
Rossano, R	1
Liuzzi, GM	1
Saleh, HA	1
Ramdan, E	1
Elmazar, MM	1
Azzazy, HME	1
Abdelnaser, A	1
Zeng, X	1
Liu, X	1
Bao, H	1
Moon, SJ	1
Jhun, J	1
Ryu, J	1
Kwon, JY	1
Kim, SY	2
Jung, K	1
Cho, ML	1
Min, JK	1
Genova, E	1
Apollonio, M	1
Decorti, G	1
Tesser, A	1
Tommasini, A	1
Stocco, G	1
Davuljigari, CB	1
Ekuban, FA	1
Zong, C	1
Fergany, AAM	1
Morikawa, K	1
Ichihara, G	1
Petkovic, M	1
Leal, EC	1
Alves, I	1
Bose, C	1
Palade, PT	1
Singh, P	1
Awasthi, S	1
Børsheim, E	1
Dalgaard, LT	1
Singh, SP	1
Carvalho, E	1
Zhang, YJ	1
Wu, Q	1
Carrasco-Pozo, C	1
Tan, KN	1
Gotteland, M	1
Borges, K	1
Redondo, A	1
Chamorro, PAF	1
Riego, G	1
Leánez, S	1
Pol, O	1
Dokumacioglu, E	1
Iskender, H	1
Aktas, MS	1
Hanedan, B	1
Dokumacioglu, A	1
Sen, TM	1
Musmul, A	1
Eren, E	1
Tufekci, KU	1
Isci, KB	1
Genc, K	1
Zhu, D	1
Chen, D	1
Dong, H	1
Wu, W	1
Lu, H	1
Wu, G	1
Hou, TT	1
Yang, HY	1
Wu, QQ	1
Tian, YR	1
Jia, JP	1
Silva Rodrigues, JF	1
Silva E Silva, C	1
França Muniz, T	1
de Aquino, AF	1
Neuza da Silva Nina, L	1
Fialho Sousa, NC	1
Nascimento da Silva, LC	1
de Souza, BGGF	1
da Penha, TA	1
Abreu-Silva, AL	1
de Sá, JC	1
Soares Fernandes, E	1
Grisotto, MAG	1
Moustafa, PE	1
Abdelkader, NF	1
El Awdan, SA	1
El-Shabrawy, OA	1
Zaki, HF	1
Gao, J	1
Xiong, B	1
Zhang, B	1
Li, S	2
Huang, N	1
Zhan, G	1
Jiang, R	1
Yang, L	1
Wu, Y	2
Zhu, B	1
Yang, C	3
Luo, A	1
Maciel-Barón, LÁ	1
Morales-Rosales, SL	1
Silva-Palacios, A	1
Rodríguez-Barrera, RH	1
García-Álvarez, JA	1
Luna-López, A	1
Pérez, VI	1
Torres, C	1
Königsberg, M	2
Rakariyatham, K	1
Tang, Z	1
Han, Y	1
Wang, Q	1
Xiao, H	1
Arita, Y	1
Jeong Park, H	1
Cantillon, A	1
Verma, K	1
Menon, R	1
Getahun, D	1
Peltier, MR	1
Gao, M	1
Wu, J	2
Hu, P	1
Xu, X	1
Chen, Z	1
Huang, C	1
Santín-Márquez, R	1
Alarcón-Aguilar, A	1
López-Diazguerrero, NE	1
Chondrogianni, N	1
Mazarakis, N	1
Snibson, K	1
Licciardi, PV	1
Karagiannis, TC	1
Subedi, L	1
Cho, K	1
Park, YU	1
Choi, HJ	1
McGovern, T	1
Farahnak, S	1
Chen, M	1
Larsson, K	1
Martin, JG	2
Adner, M	1
Zhao, XD	1
Zhou, YT	1
Lu, XJ	1
Li, B	1
Cui, W	1
Li, R	1
Xie, XH	1
Ge, XL	1
Zhang, J	1
Song, XJ	1
Wang, Y	2
Guo, L	1
Nguyen, B	1
Luong, L	1
Naase, H	1
Vives, M	1
Jakaj, G	1
Finch, J	1
Boyle, J	1
Mulholland, JW	1
Kwak, JH	1
Pyo, S	1
de Luca, A	1
Athanasiou, T	1
Angelini, G	1
Anderson, J	1
Haskard, DO	1
Evans, PC	2
Sun, W	1
Tan, Y	1
Liu, Y	1
Zheng, Y	1
Lippmann, D	1
Lehmann, C	1
Florian, S	2
Barknowitz, G	1
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Mewis, I	1
Wiesner, M	1
Schreiner, M	1
Glatt, H	1
Brigelius-Flohé, R	2
Kipp, AP	2
Meijer, K	1
Vonk, RJ	1
Priebe, MG	1
Roelofsen, H	1
Maeda, S	1
Matsui, T	1
Ojima, A	1
Takeuchi, M	1
Yamagishi, S	1
Folkard, DL	1
Melchini, A	1
Traka, MH	1
Al-Bakheit, A	1
Saha, S	1
Mulholland, F	1
Watson, A	1
Mithen, RF	1
Medina, S	1
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García-Viguera, C	1
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Pan, H	1
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Yu, AC	1
Pu, M	1
Sun, C	1
Xue, R	1
Zhang, T	1
Pan, L	1
Ma, X	1
Wang, L	2
Li, D	1
Sun, CC	1
Li, SJ	1
Yang, CL	1
Xue, RL	1
Xi, YY	1
Zhao, QL	1
Li, DJ	1
Shah, SP	1
Duda, JE	1
Dwivedi, S	1
Rajasekar, N	1
Hanif, K	1
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Hernandez-Rabaza, V	1
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Holloway, PM	1
Gillespie, S	1
Becker, F	1
Vital, SA	1
Nguyen, V	1
Alexander, JS	1
Gavins, FNE	1
Zhang, JC	1
Yao, W	1
Dong, C	1
Ren, Q	1
Ma, M	1
Han, M	1
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Suganuma, H	1
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Kong, AN	1
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Yamanoi, H	1
Tsuduki, T	1
Sookwong, P	1
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Hassan, AH	1
Hussain, A	1
Harada, N	1
Kanayama, M	1
Maruyama, A	1
Yoshida, A	1
Tazumi, K	1
Hosoya, T	1
Mimura, J	1
Toki, T	1
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Trial	Phase	Enrollment	Study Type	Start Date	Status
Enhancing Nrf2 by Sulforaphane Treatment in COPD[NCT01335971]	Phase 2	89 participants (Actual)	Interventional	2010-09-30	Completed
Sulforaphane Treatment of Children With Autism Spectrum Disorder (ASD)[NCT02561481]	Phase 1/Phase 2	60 participants (Actual)	Interventional	2015-12-31	Completed
Randomized,Double-blind, Placebo-controlled, Efficacy and Safety Study of Sulforaphane in Patients With Prodromal to Mild Alzheimer's Disease[NCT04213391]		160 participants (Anticipated)	Interventional	2020-05-10	Recruiting
A Multi-center Longitudinal Cohort Study of Familial Alzheimer's Disease in China[NCT03657732]		40,000 participants (Anticipated)	Observational [Patient Registry]	2005-01-10	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

The fifth primary design variable is the change from baseline in expression of Aldo-Keto Reductase Family 1 Member C1 (AKR1C1) in bronchial epithelial cells (BEC) at 4 weeks. Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change From Baseline in Bronchial Epithelial Cell Expression of AKR1C3 at 4 Weeks

Intervention	fold change (Median)
Placebo	1.45
Sulforaphane 25	1.08
Sulforaphane 150	0.79

The sixth primary design variable is the change from baseline in expression of Aldo-Keto Reductase Family 1 Member C3 (AKR1C3) in bronchial epithelial cells (BEC) at 4 weeks. Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change From Baseline in Bronchial Epithelial Cell Expression of HO1 at 4 Weeks

Intervention	fold change (Median)
Placebo	1.10
Sulforaphane 25	1.38
Sulforaphane 150	0.87

The fourth primary design variable is the change from baseline in expression of Heme Oxygenase 1 (HO1) in bronchial epithelial cells (BEC) at 4 weeks. Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change From Baseline in Bronchial Epithelial Cell Expression of Nrf2 at 4 Weeks

Intervention	fold change (Median)
Placebo	1.05
Sulforaphane 25	1.12
Sulforaphane 150	0.93

The second primary design variable is the change from baseline in nuclear factor erythroid 2 like 2 (Nrf2) expression in bronchial epithelial cells (BEC) at 4 weeks by analysing Nrf2 protein. Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Fold-change in Isoprostane Concentrations (Follow-up to Baseline)

Intervention	fold change (Median)
Placebo	1.09
Sulforaphane 25	1.06
Sulforaphane 150	1.06

Isoprostane, an oxidant stress indicator, was measured in expired breath condensate at baseline and 4 weeks. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change From Baseline in Alveolar Macrophage Expression of Nrf2 and Associated Genes at 4 Weeks

Intervention	fold change (Median)
Placebo	1.18
Sulforaphane 25	0.83
Sulforaphane 150	0.64

The first primary design variable is the change from baseline in nuclear factor erythroid 2 like 2 (Nrf2) expression in alveolar macrophages (AM) at 4 weeks by analysing Nrf2 protein and expression of a panel of Nrf2 regulated genes.Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change From Baseline in Bronchial Epithelial Cell Expression of NQ01 and Keap1 at 4 Weeks

Intervention	fold change (Median)
	NQ01	HO1	AKR1C1	AKR1C3	Nrf2	Keap1
Placebo	0.80	0.90	0.81	1.03	1.14	0.94
Sulforaphane 150	0.94	1.06	0.71	0.87	1.13	1.06
Sulforaphane 25	1.03	0.98	1.13	1.02	1.05	0.99

The third primary design variable is the change from baseline in NAD(P)H Quinone Dehydrogenase 1 (NQ01) and Kelch Like ECH Associated Protein 1 (Keap1) expression in bronchial epithelial cells (BEC) at 4 weeks. Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage for primary outcome data. (NCT01335971)
Timeframe: Baseline and 4 weeks

Fold-change in Inflammatory Marker Concentrations in Bronchial Alveolar Lavage (Follow-up to Baseline) by Treatment Group

Intervention	fold change (Median)
	NQ01	KEAP1
Placebo	1.09	1.12
Sulforaphane 150	0.96	0.87
Sulforaphane 25	1.12	1.39

Inflammatory markers were measured in bronchial alveolar lavage samples at baseline and 4 weeks in the participants of this trial who had bronchoalveolar lavage samples obtained.Three participants - one from each treatment group - were unable to complete follow-up bronchoalveolar lavage. (NCT01335971)
Timeframe: Baseline and 4 weeks

Fold-change in Plasma Inflammatory Marker Concentrations (Follow-up to Baseline)

Intervention	fold change (Median)
	Interleukin-8 (pg/mg)	Secretory leukoprotease inhibitor (pg/mg)
Placebo	1.22	1.51
Sulforaphane 150	1.11	1.12
Sulforaphane 25	0.94	1.09

Inflammatory markers were measured in plasma at baseline and 4 weeks. Thiobarbituric acid reactive substances were measured in nmol malondialdehyde (MDA)/mL. (NCT01335971)
Timeframe: Baseline and 4 weeks

Fold-change in Serum Inflammatory Marker Concentrations (Follow-up to Baseline)

Intervention	fold change (Median)
	Isoprostane (ng/mg)	Thiobarbituric acid reactive substances	Total antioxidants (mM Trolox equivalents/L)
Placebo	0.89	0.96	0.97
Sulforaphane 150	0.88	1.06	0.97
Sulforaphane 25	0.90	1.05	0.92

Inflammatory markers were measured in serum samples derived from venipuncture at baseline and 4 weeks in the serum of the participants of the trial. (NCT01335971)
Timeframe: Baseline and 4 weeks

Change in Ohio Autism Clinical Impressions Scale - Improvement (OACIS-I) Average Score From Baseline

Intervention	fold change (Median)
	C-reactive protein (mg/L)	Interleukin-6 (pg/mL)	Interleukin-8 (pg/mL)
Placebo	0.99	0.75	1.06
Sulforaphane 150	1.01	1.12	1.03
Sulforaphane 25	0.90	0.90	1.04

The Ohio Autism Clinical Impressions Scale-Severity (OACIS-S) rates severity of symptoms in 10 categories: general level of autism, social interaction, aberrant and repetitive behavior, verbal and nonverbal communication, hyperactivity, anxiety, sensory sensitivities and restricted and narrow interests. Each category is rated from 1 (normal) to 7 (most severe). The OACIS-S was a reference at follow up visits when the OACIS-Improvement was compared to the OACIS-S, from 1 to 7: 4 was no change; 3 to 1 minimal to marked improvement and 5 to 7 minimal to marked worsening. The numerical score of the OACIS-S is independent and unrelated quantitatively to the OACIS-I. For analysis, the OACIS-I general score and subscale values were recoded, in which 4 (no change) was recoded as 0; 3 to 1 were recoded as +1 to +3 to denote improvement, and 5 to 7 were recoded as -1 to -3 for worsening. (NCT02561481)
Timeframe: 7 weeks, 15 weeks, 22 weeks, 30 weeks, 36 weeks

Change in Total Aberrant Behavior Checklist Score From Baseline

Intervention	score on a scale (Mean)
	7 weeks	15 weeks	22 weeks	30 weeks	36 weeks
Placebo	0.28	0.33	0.59	0.69	0.29
Sulforaphane	0.28	0.28	0.47	0.47	0.29

Aberrant Behavior Checklist (ABC) is a 58 item scale that primarily evaluates how aberrant or abnormal a patient's daily behaviors are. The items evaluate behaviors as they pertain to irritability, lethargy/social withdrawal, stereotypic behavior, hyperactivity/noncompliance, and inappropriate speech. Each item is scored on a scale of 0 to 3, with 0 being better outcome and 3 being worse outcome. The score from each item is added up to calculate a total score. This outcome describes change in total ABC score from baseline at each follow up visit. The scores from all items are added to calculate a total score (0 to 174). This outcome describes change in total ABC score from baseline at each follow up visit. (NCT02561481)
Timeframe: 7 weeks, 15 weeks, 22 weeks, 30 weeks, 36 weeks

Change in Total SRS-2 Score From Baseline

Intervention	score on a scale (Mean)
	7 weeks	15 weeks	22 weeks	30 weeks	36 weeks
Placebo	-16.23	-11.68	-22.4	-10.29	-7.8
Sulforaphane	-6	-22.6	-36.33	-22.8	1.14

The Social Responsiveness Scale-2 (SRS-2) is a 65-item scale that measures total scores as well as subscales: four social behaviors (awareness, cognition, communication and motivation) and autistic mannerisms. Each item is rated from 1 to 4 (not true to almost always true) on worksheets that are blinded to the rater with respect to values. Total and subscale scores are calculated as raw scores and can be converted to T-scores. Raw scores (range 0-180) are reported here (unadjusted for general population, since all children had ASD). Higher or lower values at follow up visits compared to baseline indicated worsening or improvement, respectively. (NCT02561481)
Timeframe: 7 weeks, 15 weeks, 22 weeks, 30 weeks, 36 weeks

Comparison of Free Reduced Glutathione (GSH), Total GSH, Oxidized Glutathione (GSSG) at Week 0 and 15

Intervention	score on a scale (Mean)
	7 weeks	15 weeks	22 weeks	30 weeks	36 weeks
Placebo	-8.06	-7.92	-13.67	-18.59	-19.59
Sulforaphane	1.14	-16.86	-14.61	-19.83	0.80

F-statistic calculated by comparison of Free Reduced GSH, Total GSH and oxidized Glutathione (GSSG) of Week 15 to Week 0. (NCT02561481)
Timeframe: Week 0 and Week 15

Cox-2

Intervention	F-statistic (Number)
	Free Reduced GSH	Total GSH	GSSG
Placebo	0.11	0.08	0.46
Sulforaphane	1.51	0.00	1.97

Cox-2 (cyclooxygenase-2): a nuclear factor-kappa B - regulated inflammatory biomarker. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

Dithiocarbamate Plasma Concentration Detected by Cyclocondensation at Each Visit

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	-0.20	0.16	-0.17
Sulforaphane	0.14	-0.07	-0.46

Sulforaphane (and other isothiocyanates, ITC) are conjugated by glutathione (GSH) which then undergoes further enzymatic modifications to give rise sequentially to the cysteinylglycine-, cysteine- and N-acetylcysteine-ITC conjugates, all of which are dithiocarbamates (DTC) and are detected in the cyclocondensation reaction-HPLC assay. (NCT02561481)
Timeframe: Week 0, Week 7, Week 15, Week 22, Week 30, Week 36

Free GSH:GSSG and Total GSH:GSSG Ratios at Week 15

Intervention	nmol DTC (Dithiocarbamates)/ml (Mean)
	Week 0	Week 7	Week 15	Week 22	Week 30	Week 36
Placebo	0.006	0.003	0.005	0.205	0.214	0.008
Sulforaphane	0.007	0.299	0.329	0.248	0.165	0.015

Ratios of free GSH:GSSG and total GSH:GSSG were calculated by obtaining ratios of f-statistic scores from baseline to week 15 between free reduced GSH and GSSG and between total GSH and GSSG. (NCT02561481)
Timeframe: Week 15

HO-1 (Heme Oxygenase 1)

Intervention	F-statistic (Number)
	Free GSH:GSSG	Total GSH:GSSG
Placebo	0.87	0.03
Sulforaphane	12.72	5.16

HO-1 (heme oxygenase 1): an essential and Nrf2-dependent enzyme in heme catabolism. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

HSP27

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	0.27	0.55	0.30
Sulforaphane	0.10	0.74	0.74

HSP27 (Heat shock protein 27) was examined because it is upregulated by SF in vitro. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30.

HSP70

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	-0.13	-0.83	-0.58
Sulforaphane	0.21	0.21	-0.47

HSP70 (Heat shock protein 70) was examined because it is upregulated by SF in vitro. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

IL-1β

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	0.99	1.14	1.20
Sulforaphane	1.11	1.33	1.23

IL-1β: Interleukin-1 beta cytokine gene expression, a nuclear factor-kappa B - regulated inflammatory biomarker. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

IL-6

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	1.14	1.47	1.59
Sulforaphane	0.90	1.45	1.50

IL-6 (interleukin 6) cytokine gene expression, a nuclear factor-kappa B - regulated inflammatory biomarker. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

NQO1: NAD(P)H:Quinone Oxidoreductase-1

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	1.82	1.87	2.08
Sulforaphane	1.76	2.05	1.99

Cytoprotective enzyme regulated by nuclear factor erythroid 2-related factor 2 (Nrf2), the master regulator of cellular redox homeostasis and an inhibitor of a key pro-inflammatory pathway, of which both functions are critical factors in the neuropathology of ASD. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

OACIS-I Response Rate on Aberrant Behaviors Subscale

Intervention	log fold change (Mean)
	Week 0 (baseline)	Week 15	Week 30
Placebo	2.25	2.14	2.13
Sulforaphane	2.23	2.19	2.15

See above in the primary outcome measure for a description of OACIS-I scale. This section describes the change from baseline of the OACIS-I subdomain of aberrant behaviors. This subdomain has a range of 1 to 7 - 1 is extremely improved from baseline, 7 is extremely worse from baseline, and 4 is no change. For analysis, the OACIS-I general score and subscale values were recoded, in which 4 (no change) was recoded as 0; 3 to 1 were recoded as +1 to +3 to denote improvement, and 5 to 7 were recoded as -1 to -3 for worsening. (NCT02561481)
Timeframe: 7 weeks, 15 weeks, 22 weeks, 30 weeks, 36 weeks

OACIS-I Response Rate on Social Communication Subscale

Intervention	score on a scale (Mean)
	7 weeks	15 weeks	22 weeks	30 weeks	36 weeks
Placebo	0.28	0.33	0.53	0.59	0.14
Sulforaphane	0.06	0.22	0.59	0.63	0.14

See above in the primary outcome measure for a description of OACIS-I scale. This section describes the change from baseline of the OACIS-I subdomain of social communication. This subdomain has a range of 1 to 7 - 1 is extremely improved from baseline, 7 is extremely worse from baseline, and 4 is no change. For analysis, the OACIS-I general score and subscale values were recoded, in which 4 (no change) was recoded as 0; 3 to 1 were recoded as +1 to +3 to denote improvement, and 5 to 7 were recoded as -1 to -3 for worsening. (NCT02561481)
Timeframe: 7 weeks, 15 weeks, 22 weeks, 30 weeks, 36 weeks

TNF-α

Intervention	score on a scale (Mean)
	7 weeks	15 weeks	22 weeks	30 weeks	36 weeks
Placebo	0.56	0.56	1.35	1.25	0.61
Sulforaphane	0.33	0.44	0.65	0.94	0.32

TNF-α (Tumor necrosis factor alpha), a cytokine as inflammatory biomarker. Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

xCT

Intervention	log fold change (Mean)
	Week 0	Week 15	Week 30
Placebo	0.91	1.08	1.10
Sulforaphane	0.70	0.98	1.17

xCT (SLC7A11): Cystine/glutamate antiporter encoded by the SLC7A11 gene.Total cellular RNA was isolated from peripheral blood mononuclear cells (PBMCs) and complementary DNAs (cDNA) were synthesized. Quantitative real-time PCR analysis was performed using the Applied Biosystems QuantStudio™ 3 Real-Time PCR System (Thermo Fisher Scientiﬁc, Waltham, MA, USA). Relative mRNA expression was normalized to GAPDH. Gene expression was calculated using the comparative 2-ΔΔCT method. (NCT02561481)
Timeframe: Week 0, Week 15, Week 30

Article	Year
Inhibitory effects of phytochemicals on NLRP3 inflammasome activation: A review. Phytomedicine : international journal of phytotherapy and phytopharmacology, 2020, Aug-15, Volume: 75 Topics: Animals; Cardiovascular Diseases; Central Nervous System Diseases; Curcumin; Humans; Inflammasomes;	2020
Molecular changes associated with the anticancer effect of sulforaphane against Ehrlich solid tumour in mice. Journal of biochemical and molecular toxicology, 2021, Volume: 35, Issue:2 Topics: Animals; Anticarcinogenic Agents; Carcinoma, Ehrlich Tumor; Epigenesis, Genetic; Female; Inflammatio	2021
Sulforaphane - role in aging and neurodegeneration. GeroScience, 2019, Volume: 41, Issue:5 Topics: Aging; Animals; Antioxidants; Epigenesis, Genetic; Humans; Inflammation; Isothiocyanates; Kelch-Like	2019
The potential use of l-sulforaphane for the treatment of chronic inflammatory diseases: A review of the clinical evidence. Clinical nutrition (Edinburgh, Scotland), 2020, Volume: 39, Issue:3 Topics: Anti-Inflammatory Agents; Chronic Disease; Humans; Inflammation; Isothiocyanates; Sulfoxides	2020

Article	Year
Protective effects of sulforaphane on inflammation, oxidative stress and intestinal dysbacteriosis induced by triphenyltin in Cyprinus carpio haematopterus. Fish & shellfish immunology, 2023, Volume: 142 Topics: Animals; Antioxidants; Carps; Dysbiosis; Inflammation; Oxidative Stress	2023
Compartmentalization of anti-oxidant and anti-inflammatory gene expression in current and former smokers with COPD. Respiratory research, 2019, Aug-20, Volume: 20, Issue:1 Topics: Aged; Antioxidants; Bronchi; Double-Blind Method; Epithelium; Female; Gene Expression; Humans; Infla	2019
Sulforaphane as an adjunctive treatment for irritability in children with autism spectrum disorder: A randomized, double-blind, placebo-controlled clinical trial. Psychiatry and clinical neurosciences, 2020, Volume: 74, Issue:7 Topics: Anti-Inflammatory Agents; Antioxidants; Antipsychotic Agents; Autism Spectrum Disorder; Child; Child	2020

Article	Year
New Monocyclic, Bicyclic, and Tricyclic Ethynylcyanodienones as Activators of the Keap1/Nrf2/ARE Pathway and Inhibitors of Inducible Nitric Oxide Synthase. Journal of medicinal chemistry, 2015, Jun-11, Volume: 58, Issue:11 Topics: Adaptor Proteins, Signal Transducing; Alkynes; Animals; Anti-Inflammatory Agents; Antineoplastic Age	2015
Synthesis and assessment of phenylacrylamide derivatives as potential anti-oxidant and anti-inflammatory agents. European journal of medicinal chemistry, 2019, Oct-15, Volume: 180 Topics: Acrylamide; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Cell Survival; Dose-Response Rela	2019
Attenuation of experimentally induced atopic dermatitis in mice by sulforaphane: effect on inflammation and apoptosis. Toxicology mechanisms and methods, 2022, Volume: 32, Issue:3 Topics: Animals; Apoptosis; Cytokines; Dermatitis, Atopic; Disease Models, Animal; Inflammation; Isothiocyan	2022
Membrane Vesicles for Nanoencapsulated Sulforaphane Increased Their Anti-Inflammatory Role on an In Vitro Human Macrophage Model. International journal of molecular sciences, 2022, Feb-09, Volume: 23, Issue:4 Topics: Anti-Inflammatory Agents; Brassica; Cell Line, Tumor; Cells, Cultured; HL-60 Cells; Humans; Inflamma	2022
Sulforaphane reduces pro-inflammatory response to palmitic acid in monocytes and adipose tissue macrophages. The Journal of nutritional biochemistry, 2022, Volume: 104 Topics: Adipose Tissue; Humans; Inflammasomes; Inflammation; Interleukin-1beta; Isothiocyanates; Lipopolysac	2022
Sulforaphane reduces obesity by reversing leptin resistance. eLife, 2022, 03-24, Volume: 11 Topics: Animals; Inflammation; Isothiocyanates; Leptin; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Ob	2022
Differential Expression of miRNAs in Trichloroethene-Mediated Inflammatory/Autoimmune Response and Its Modulation by Sulforaphane: Delineating the Role of miRNA-21 and miRNA-690. Frontiers in immunology, 2022, Volume: 13 Topics: Animals; Antioxidants; Autoimmune Diseases; Autoimmunity; Corn Oil; Female; Inflammation; Isothiocya	2022
The Protective Effect of Sulforaphane on ER-induced Apoptosis and Inflammation in Necrotizing Enterocolitis Mice. Combinatorial chemistry & high throughput screening, 2023, Volume: 26, Issue:6 Topics: Animals; Apoptosis; Disease Models, Animal; Enterocolitis, Necrotizing; Inflammation; Interleukin-10	2023
Essential role of Nrf2 in sulforaphane-induced protection against angiotensin II-induced aortic injury. Life sciences, 2022, Oct-01, Volume: 306 Topics: Angiotensin II; Animals; Glycogen Synthase Kinase 3 beta; Inflammation; Isothiocyanates; Mice; Mice,	2022
Sulforaphane alleviated vascular remodeling in hypoxic pulmonary hypertension via inhibiting inflammation and oxidative stress. The Journal of nutritional biochemistry, 2023, Volume: 111 Topics: Animals; Cell Proliferation; Endothelial Cells; Hypertension, Pulmonary; Hypoxia; Inflammation; Isot	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane reduces lipopolysaccharide-induced inflammation and enhances myogenic differentiation of mouse embryonic myoblasts via the toll-like receptor 4 and NLRP3 pathways. Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 2023, Volume: 32, Issue:4 Topics: Animals; Cell Differentiation; Inflammasomes; Inflammation; Lipopolysaccharides; Mice; Myoblasts; NL	2023
Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity. Cardiovascular toxicology, 2023, Volume: 23, Issue:1 Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cardiotoxicity; Catalase; Chemical and Drug Induced	2023
Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut-Liver Axis. Nutrients, 2023, Feb-01, Volume: 15, Issue:3 Topics: Animals; Diet, High-Fat; Fructose; Inflammation; Lipopolysaccharides; Liver; Mice; Mice, Inbred C57B	2023
Sulforaphane Reduces the Chronic Inflammatory Immune Response of Human Dendritic Cells. Nutrients, 2023, Jul-31, Volume: 15, Issue:15 Topics: Cell Differentiation; Cells, Cultured; Cytokines; Dendritic Cells; Humans; Immunity; Inflammation; I	2023
Sulforaphane alleviates psoriasis by enhancing antioxidant defense through KEAP1-NRF2 Pathway activation and attenuating inflammatory signaling. Cell death & disease, 2023, Nov-25, Volume: 14, Issue:11 Topics: Animals; Antioxidants; Cytokines; Disease Models, Animal; Humans; Inflammation; Kelch-Like ECH-Assoc	2023
Enhancing the Nrf2 Antioxidant Signaling Provides Protection Against Trichloroethene-mediated Inflammation and Autoimmune Response. Toxicological sciences : an official journal of the Society of Toxicology, 2020, 05-01, Volume: 175, Issue:1 Topics: Acetates; Animals; Antioxidants; Apoptosis; Autoimmunity; Female; Heme Oxygenase-1; Humans; Inflamma	2020
Biomarker Exploration in Human Peripheral Blood Mononuclear Cells for Monitoring Sulforaphane Treatment Responses in Autism Spectrum Disorder. Scientific reports, 2020, 04-02, Volume: 10, Issue:1 Topics: Autism Spectrum Disorder; Cells, Cultured; Child; Cytokines; Humans; Inflammation; Isothiocyanates;	2020
Sulforaphane reduces intracellular survival of Staphylococcus aureus in macrophages through inhibition of JNK and p38 MAPK‑induced inflammation. International journal of molecular medicine, 2020, Volume: 45, Issue:6 Topics: Animals; Anti-Bacterial Agents; Apoptosis; Gene Expression Regulation; Humans; Inflammation; Isothio	2020
Risk of neuropsychiatric disorders in offspring of COVID-19-infected pregnant women and nutritional intervention. European archives of psychiatry and clinical neuroscience, 2021, Volume: 271, Issue:2 Topics: Autism Spectrum Disorder; C-Reactive Protein; COVID-19; Dietary Supplements; Female; Gestational Age	2021
Comparative effectiveness of 4 natural and chemical activators of Nrf2 on inflammation, oxidative stress, macrophage polarization, and bactericidal activity in an in vitro macrophage infection model. PloS one, 2020, Volume: 15, Issue:6 Topics: Anti-Inflammatory Agents; Antioxidants; Dimethyl Fumarate; Escherichia coli; Escherichia coli Infect	2020
Acute antioxidant and cytoprotective effects of sulforaphane in brain endothelial cells and astrocytes during inflammation and excitotoxicity. Pharmacology research & perspectives, 2020, Volume: 8, Issue:4 Topics: Animals; Animals, Newborn; Antioxidants; Apoptosis; Astrocytes; Brain; Cells, Cultured; Endothelial	2020
Dietary polyacetylene falcarinol upregulated intestinal heme oxygenase-1 and modified plasma cytokine profile in late phase lipopolysaccharide-induced acute inflammation in CB57BL/6 mice. Nutrition research (New York, N.Y.), 2020, Volume: 80 Topics: Animals; Cytokines; Dietary Supplements; Diynes; Fatty Acids, Unsaturated; Fatty Alcohols; Granulocy	2020
Sulforaphane prevents type 2 diabetes-induced nephropathy via AMPK-mediated activation of lipid metabolic pathways and Nrf2 antioxidative function. Clinical science (London, England : 1979), 2020, 09-30, Volume: 134, Issue:18 Topics: AMP-Activated Protein Kinases; Animals; Antioxidants; Diabetes Mellitus, Type 2; Diabetic Nephropath	2020
Sulforaphane mitigates LPS-induced neuroinflammation through modulation of Cezanne/NF-κB signalling. Life sciences, 2020, Dec-01, Volume: 262 Topics: Animals; Cytokines; Endopeptidases; Hippocampus; Inflammation; Isothiocyanates; Lipopolysaccharides;	2020
Transcription Factor Nrf2 as a Potential Therapeutic Target for Prevention of Cytokine Storm in COVID-19 Patients. Biochemistry. Biokhimiia, 2020, Volume: 85, Issue:7 Topics: Animals; Antioxidants; Betacoronavirus; Catechin; Coronavirus Infections; COVID-19; COVID-19 Drug Tr	2020
Neuroprotective potential of isothiocyanates in an in vitro model of neuroinflammation. Inflammopharmacology, 2021, Volume: 29, Issue:2 Topics: Animals; Astrocytes; Cells, Cultured; Disease Models, Animal; Dose-Response Relationship, Drug; Fema	2021
Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages. Scientific reports, 2021, 01-12, Volume: 11, Issue:1 Topics: Animals; Antibiotics, Antineoplastic; Curcumin; Doxorubicin; Immunologic Factors; Inflammation; Infl	2021
Sulforaphane suppresses lipopolysaccharide- and Pam3CysSerLys4-mediated inflammation in chronic obstructive pulmonary disease via toll-like receptors. FEBS open bio, 2021, Volume: 11, Issue:5 Topics: Aged; Anti-Inflammatory Agents; China; Female; Humans; Inflammation; Inflammation Mediators; Isothio	2021
The anti-arthritis effect of sulforaphane, an activator of Nrf2, is associated with inhibition of both B cell differentiation and the production of inflammatory cytokines. PloS one, 2021, Volume: 16, Issue:2 Topics: Animals; Arthritis, Rheumatoid; B-Lymphocytes; Cell Differentiation; Cytokines; Inflammation; Isothi	2021
In Vitro Effects of Sulforaphane on Interferon-Driven Inflammation and Exploratory Evaluation in Two Healthy Volunteers. Molecules (Basel, Switzerland), 2021, Jun-12, Volume: 26, Issue:12 Topics: Adult; Cell Line, Tumor; Female; Gene Expression; Genotype; Glutathione Transferase; Healthy Volunte	2021
Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice. International journal of molecular sciences, 2021, Jun-01, Volume: 22, Issue:11 Topics: Acrylamide; Animals; Disease Models, Animal; Humans; Inflammation; Isothiocyanates; Mice; Microglia;	2021
Dietary supplementation with sulforaphane ameliorates skin aging through activation of the Keap1-Nrf2 pathway. The Journal of nutritional biochemistry, 2021, Volume: 98 Topics: Animals; Antioxidants; Dietary Supplements; Inflammation; Isothiocyanates; Kelch-Like ECH-Associated	2021
Sulforaphane protects intestinal epithelial cells against lipopolysaccharide-induced injury by activating the AMPK/SIRT1/PGC-1ɑ pathway. Bioengineered, 2021, Volume: 12, Issue:1 Topics: AMP-Activated Protein Kinases; Apoptosis; Caco-2 Cells; Epithelial Cells; Humans; Inflammation; Inte	2021
Sulforaphane Protects against High Cholesterol-Induced Mitochondrial Bioenergetics Impairments, Inflammation, and Oxidative Stress and Preserves Pancreatic Oxidative medicine and cellular longevity, 2017, Volume: 2017 Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cells, Cultured; Cholesterol; Dietary Supplements;	2017
Treatment with Sulforaphane Produces Antinociception and Improves Morphine Effects during Inflammatory Pain in Mice. The Journal of pharmacology and experimental therapeutics, 2017, Volume: 363, Issue:3 Topics: Analgesics; Analgesics, Opioid; Animals; Chronic Pain; Drug Therapy, Combination; Freund's Adjuvant;	2017
The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene. Bratislavske lekarske listy, 2017, Volume: 118, Issue:8 Topics: Acetaminophen; Alanine Transaminase; Analgesics, Non-Narcotic; Animals; Antioxidants; Aspartate Amin	2017
Sulforaphane Inhibits Lipopolysaccharide-Induced Inflammation, Cytotoxicity, Oxidative Stress, and miR-155 Expression and Switches to Mox Phenotype through Activating Extracellular Signal-Regulated Kinase 1/2-Nuclear Factor Erythroid 2-Related Factor 2/An Frontiers in immunology, 2018, Volume: 9 Topics: Animals; Anti-Inflammatory Agents; Antioxidant Response Elements; Antioxidants; Apoptosis; Cell Line	2018
Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure. Medical science monitor : international medical journal of experimental and clinical research, 2018, Mar-12, Volume: 24 Topics: Animals; Apoptosis; Atrial Natriuretic Factor; Chronic Disease; Collagen; Cytokines; Female; Fibrosi	2018
Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice. Journal of Alzheimer's disease : JAD, 2018, Volume: 62, Issue:4 Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Cell Survival; Cerebral Cortex; Fem	2018
Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice. Journal of Alzheimer's disease : JAD, 2018, Volume: 62, Issue:4 Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Cell Survival; Cerebral Cortex; Fem	2018
Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice. Journal of Alzheimer's disease : JAD, 2018, Volume: 62, Issue:4 Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Cell Survival; Cerebral Cortex; Fem	2018
Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice. Journal of Alzheimer's disease : JAD, 2018, Volume: 62, Issue:4 Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Cell Survival; Cerebral Cortex; Fem	2018
Sulforaphane Modulates Joint Inflammation in a Murine Model of Complete Freund's Adjuvant-Induced Mono-Arthritis. Molecules (Basel, Switzerland), 2018, 04-24, Volume: 23, Issue:5 Topics: Animals; Arthritis, Experimental; Arthritis, Rheumatoid; Biomarkers; Cytokines; Disease Models, Anim	2018
Extracellular Matrix Remodeling and Modulation of Inflammation and Oxidative Stress by Sulforaphane in Experimental Diabetic Peripheral Neuropathy. Inflammation, 2018, Volume: 41, Issue:4 Topics: Animals; Anticarcinogenic Agents; Blood Glucose; Body Weight; Diabetes Mellitus, Experimental; Diabe	2018
Sulforaphane Alleviates Lipopolysaccharide-induced Spatial Learning and Memory Dysfunction in Mice: The Role of BDNF-mTOR Signaling Pathway. Neuroscience, 2018, 09-15, Volume: 388 Topics: Animals; Brain-Derived Neurotrophic Factor; Hippocampus; Inflammation; Isothiocyanates; Learning Dis	2018
The secretory phenotype of senescent astrocytes isolated from Wistar newborn rats changes with anti-inflammatory drugs, but does not have a short-term effect on neuronal mitochondrial potential. Biogerontology, 2018, Volume: 19, Issue:5 Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents; Astrocytes; Cellular Senescence; Central Nervou	2018
Synergism between luteolin and sulforaphane in anti-inflammation. Food & function, 2018, Oct-17, Volume: 9, Issue:10 Topics: Animals; Anti-Inflammatory Agents; Cyclooxygenase 2; Drug Synergism; Heme Oxygenase-1; Humans; Infla	2018
Pro- and anti-inflammatory effects of sulforaphane on placental cytokine production. Journal of reproductive immunology, 2019, Volume: 131 Topics: Adult; Cytokines; Escherichia coli; Escherichia coli Infections; Female; Humans; Inflammation; Isoth	2019
Sulforaphane triggers a functional elongation of microglial process via the Akt signal. The Journal of nutritional biochemistry, 2019, Volume: 67 Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Behavior, Animal; Cells, Cultured; Chromones; Cyto	2019
Sulforaphane-Enriched Broccoli Sprouts Pretreated by Pulsed Electric Fields Reduces Neuroinflammation and Ameliorates Scopolamine-Induced Amnesia in Mouse Brain through Its Antioxidant Ability via Nrf2-HO-1 Activation. Oxidative medicine and cellular longevity, 2019, Volume: 2019 Topics: Amnesia; Animals; Brassica; Heme Oxygenase-1; Inflammation; Isothiocyanates; Male; MAP Kinase Signal	2019
Organic dust, causing both oxidative stress and Nrf2 activation, is phagocytized by bronchial epithelial cells. American journal of physiology. Lung cellular and molecular physiology, 2019, 09-01, Volume: 317, Issue:3 Topics: Animals; Antioxidants; Bronchi; Dust; Epithelial Cells; Inflammation; Isothiocyanates; Lung; Mice; N	2019
Sulforaphane enhances the activity of the Nrf2-ARE pathway and attenuates inflammation in OxyHb-induced rat vascular smooth muscle cells. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2013, Volume: 62, Issue:9 Topics: Animals; Antioxidant Response Elements; Cells, Cultured; Heme Oxygenase-1; Inflammation; Interleukin	2013
Sulforaphane ameliorates the development of experimental autoimmune encephalomyelitis by antagonizing oxidative stress and Th17-related inflammation in mice. Experimental neurology, 2013, Volume: 250 Topics: Animals; Antioxidants; Blotting, Western; Encephalomyelitis, Autoimmune, Experimental; Enzyme-Linked	2013
Sulforaphane pretreatment prevents systemic inflammation and renal injury in response to cardiopulmonary bypass. The Journal of thoracic and cardiovascular surgery, 2014, Volume: 148, Issue:2 Topics: Acute Kidney Injury; Animals; Anti-Inflammatory Agents; Cardiopulmonary Bypass; Cells, Cultured; Dis	2014
Sulforaphane attenuation of type 2 diabetes-induced aortic damage was associated with the upregulation of Nrf2 expression and function. Oxidative medicine and cellular longevity, 2014, Volume: 2014 Topics: Animals; Aorta; Apoptosis; Cell Proliferation; Diabetes Mellitus, Experimental; Diabetes Mellitus, T	2014
Glucosinolates from pak choi and broccoli induce enzymes and inhibit inflammation and colon cancer differently. Food & function, 2014, Volume: 5, Issue:6 Topics: Animals; Anticarcinogenic Agents; Basic Helix-Loop-Helix Transcription Factors; Brassica; Colon; Col	2014
Cell-based screening assay for anti-inflammatory activity of bioactive compounds. Food chemistry, 2015, Jan-01, Volume: 166 Topics: Anti-Inflammatory Agents; HEK293 Cells; Humans; Inflammation; Isothiocyanates; NF-kappa B; Sulfoxide	2015
Sulforaphane inhibits advanced glycation end product-induced pericyte damage by reducing expression of receptor for advanced glycation end products. Nutrition research (New York, N.Y.), 2014, Volume: 34, Issue:9 Topics: Animals; Apoptosis; Brassicaceae; Cattle; Cells, Cultured; Chemokine CCL2; Diabetic Retinopathy; DNA	2014
Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. Molecular nutrition & food research, 2014, Volume: 58, Issue:12 Topics: Brassica; Cell Line; Chromatography, Liquid; Cytokines; Humans; Inflammation; Isothiocyanates; Leuko	2014
The intake of broccoli sprouts modulates the inflammatory and vascular prostanoids but not the oxidative stress-related isoprostanes in healthy humans. Food chemistry, 2015, Apr-15, Volume: 173 Topics: Adult; Ascorbic Acid; Biomarkers; Brassica; Chromatography, High Pressure Liquid; Cross-Over Studies	2015
Sulforaphane protects rodent retinas against ischemia-reperfusion injury through the activation of the Nrf2/HO-1 antioxidant pathway. PloS one, 2014, Volume: 9, Issue:12 Topics: Amacrine Cells; Animals; Antioxidants; Apoptosis; Disease Models, Animal; Heme Oxygenase-1; Inflamma	2014
Sulforaphane alleviates muscular dystrophy in mdx mice by activation of Nrf2. Journal of applied physiology (Bethesda, Md. : 1985), 2015, Jan-15, Volume: 118, Issue:2 Topics: Animals; Anticarcinogenic Agents; Antioxidant Response Elements; Drug Evaluation, Preclinical; Gene	2015
Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling Pathway. The Journal of biological chemistry, 2015, Jul-17, Volume: 290, Issue:29 Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Dystrophin; Gene Deletion; Heme Oxygenase-1; Inflam	2015
Dietary modifications in Parkinson's disease: A neuroprotective intervention? Medical hypotheses, 2015, Volume: 85, Issue:6 Topics: Animals; Antioxidants; Curcumin; Diet; Ergothioneine; Fragaria; Humans; Inflammation; Isothiocyanate	2015
Sulforaphane Ameliorates Okadaic Acid-Induced Memory Impairment in Rats by Activating the Nrf2/HO-1 Antioxidant Pathway. Molecular neurobiology, 2016, Volume: 53, Issue:8 Topics: Animals; Antioxidants; Apoptosis; Biomarkers; Cell Line, Tumor; Cell Survival; Glutamate-Cysteine Li	2016
Neuroinflammation increases GABAergic tone and impairs cognitive and motor function in hyperammonemia by increasing GAT-3 membrane expression. Reversal by sulforaphane by promoting M2 polarization of microglia. Journal of neuroinflammation, 2016, Apr-18, Volume: 13, Issue:1 Topics: Animals; Anti-Inflammatory Agents; Blotting, Western; Cell Membrane; Cerebellum; Disease Models, Ani	2016
Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways. Vascular pharmacology, 2016, Volume: 85 Topics: Adolescent; Adult; Animals; Anti-Inflammatory Agents; Antioxidants; Brain; Cell Line; Disease Models	2016
Prophylactic effects of sulforaphane on depression-like behavior and dendritic changes in mice after inflammation. The Journal of nutritional biochemistry, 2017, Volume: 39 Topics: Animals; Behavior, Animal; Brain-Derived Neurotrophic Factor; Brassica; Depression; Disease Models,	2017
Inflammation and airway hyperresponsiveness after chlorine exposure are prolonged by Nrf2 deficiency in mice. Free radical biology & medicine, 2017, Volume: 102 Topics: Animals; Bronchoalveolar Lavage; Buthionine Sulfoximine; Chlorine; Gene Expression Regulation; Gluta	2017
Sulforaphane suppressed LPS-induced inflammation in mouse peritoneal macrophages through Nrf2 dependent pathway. Biochemical pharmacology, 2008, Oct-15, Volume: 76, Issue:8 Topics: Animals; Anticarcinogenic Agents; Dinoprostone; Inflammation; Interleukin-1beta; Isothiocyanates; Li	2008
Sulforaphane suppresses ultraviolet B-induced inflammation in HaCaT keratinocytes and HR-1 hairless mice. The Journal of nutritional biochemistry, 2010, Volume: 21, Issue:8 Topics: Animals; Base Sequence; Cell Line; Cell Proliferation; DNA Primers; Enzyme-Linked Immunosorbent Assa	2010
Sulforaphane suppresses LPS-induced inflammation in primary rat microglia. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2010, Volume: 59, Issue:6 Topics: Animals; Anti-Inflammatory Agents; Blotting, Western; Cells, Cultured; Cytokines; Extracellular Sign	2010
Anti-carcinogenic effects of sulforaphane in association with its apoptosis-inducing and anti-inflammatory properties in human cervical cancer cells. Cancer epidemiology, 2011, Volume: 35, Issue:3 Topics: Anticarcinogenic Agents; Antimetabolites, Antineoplastic; Apoptosis; Cell Survival; Cyclooxygenase 2	2011
Nrf2 regulates ferroportin 1-mediated iron efflux and counteracts lipopolysaccharide-induced ferroportin 1 mRNA suppression in macrophages. Archives of biochemistry and biophysics, 2011, Apr-01, Volume: 508, Issue:1 Topics: Animals; Antimicrobial Cationic Peptides; Cation Transport Proteins; Cell Line; Down-Regulation; Enz	2011
Inactivation of tautomerase activity of macrophage migration inhibitory factor by sulforaphane: a potential biomarker for anti-inflammatory intervention. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2011, Volume: 20, Issue:7 Topics: Animals; Biomarkers; Enzyme Inhibitors; Humans; Inflammation; Intramolecular Oxidoreductases; Isothi	2011
Sulforaphane, a natural constituent of broccoli, prevents cell death and inflammation in nephropathy. The Journal of nutritional biochemistry, 2012, Volume: 23, Issue:5 Topics: Animals; Antineoplastic Agents; Brassica; Cell Death; Cisplatin; Inflammation; Isothiocyanates; JNK	2012
Sulforaphane prevents microcystin-LR-induced oxidative damage and apoptosis in BALB/c mice. Toxicology and applied pharmacology, 2011, Aug-15, Volume: 255, Issue:1 Topics: Animals; Apoptosis; Cytochrome P-450 CYP2E1; Glutathione; Inflammation; Isothiocyanates; Liver; Male	2011
Glutathione peroxidase-2 and selenium decreased inflammation and tumors in a mouse model of inflammation-associated carcinogenesis whereas sulforaphane effects differed with selenium supply. Carcinogenesis, 2012, Volume: 33, Issue:3 Topics: Animals; Apoptosis; Azoxymethane; Cell Transformation, Neoplastic; Colitis; Colon; Colonic Neoplasms	2012

sulforaphane and Inflammation