sulforaphane has been researched along with Innate Inflammatory Response in 82 studies
sulforaphane: from Cardaria draba L.
sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.
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) |
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 |
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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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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.
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
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
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
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
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
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
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
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
Intervention | log fold change (Mean) | ||
---|---|---|---|
Week 0 | Week 15 | Week 30 | |
Placebo | 0.40 | 0.30 | 0.27 |
Sulforaphane | 0.24 | 0.25 | 0.24 |
4 reviews available for sulforaphane and Innate Inflammatory Response
Article | Year |
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Inhibitory effects of phytochemicals on NLRP3 inflammasome activation: A review.
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.
Topics: Animals; Anticarcinogenic Agents; Carcinoma, Ehrlich Tumor; Epigenesis, Genetic; Female; Inflammatio | 2021 |
Sulforaphane - role in aging and neurodegeneration.
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.
Topics: Anti-Inflammatory Agents; Chronic Disease; Humans; Inflammation; Isothiocyanates; Sulfoxides | 2020 |
3 trials available for sulforaphane and Innate Inflammatory Response
Article | Year |
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Protective effects of sulforaphane on inflammation, oxidative stress and intestinal dysbacteriosis induced by triphenyltin in Cyprinus carpio haematopterus.
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.
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.
Topics: Anti-Inflammatory Agents; Antioxidants; Antipsychotic Agents; Autism Spectrum Disorder; Child; Child | 2020 |
75 other studies available for sulforaphane and Innate Inflammatory Response
Article | Year |
---|---|
New Monocyclic, Bicyclic, and Tricyclic Ethynylcyanodienones as Activators of the Keap1/Nrf2/ARE Pathway and Inhibitors of Inducible Nitric Oxide Synthase.
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.
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.
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.
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.
Topics: Adipose Tissue; Humans; Inflammasomes; Inflammation; Interleukin-1beta; Isothiocyanates; Lipopolysac | 2022 |
Sulforaphane reduces obesity by reversing leptin resistance.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Adult; Cell Line, Tumor; Female; Gene Expression; Genotype; Glutathione Transferase; Healthy Volunte | 2021 |
Nrf2 Activation Attenuates Acrylamide-Induced Neuropathy in Mice.
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.
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.
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
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents; Astrocytes; Cellular Senescence; Central Nervou | 2018 |
Synergism between luteolin and sulforaphane in anti-inflammation.
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.
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.
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.
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.
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.
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.
Topics: Animals; Antioxidants; Blotting, Western; Encephalomyelitis, Autoimmune, Experimental; Enzyme-Linked | 2013 |
Sulforaphane pretreatment prevents systemic inflammation and renal injury in response to cardiopulmonary bypass.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Dystrophin; Gene Deletion; Heme Oxygenase-1; Inflam | 2015 |
Dietary modifications in Parkinson's disease: A neuroprotective intervention?
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.
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.
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.
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.
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.
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.
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.
Topics: Animals; Base Sequence; Cell Line; Cell Proliferation; DNA Primers; Enzyme-Linked Immunosorbent Assa | 2010 |
Sulforaphane suppresses LPS-induced inflammation in primary rat microglia.
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.
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.
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.
Topics: Animals; Biomarkers; Enzyme Inhibitors; Humans; Inflammation; Intramolecular Oxidoreductases; Isothi | 2011 |
Sulforaphane, a natural constituent of broccoli, prevents cell death and inflammation in nephropathy.
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.
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.
Topics: Animals; Apoptosis; Azoxymethane; Cell Transformation, Neoplastic; Colitis; Colon; Colonic Neoplasms | 2012 |