rosmarinic-acid has been researched along with Body-Weight* in 13 studies
1 review(s) available for rosmarinic-acid and Body-Weight
1 trial(s) available for rosmarinic-acid and Body-Weight
12 other study(ies) available for rosmarinic-acid and Body-Weight
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Protective effect of rosmarinic acid-rich extract from Trichodesma khasianum Clarke against microbiota dysbiosis in high-fat diet-fed obese mice.
Hypertrophy of adipose tissues and dysbiosis are hallmarks of obesity. Although drugs are applied for obesity treatment, side effects limit their use. The anti-obesity capacity of rosmarinic acid (RA) has been documented. Trichodesma khasianum Clarke is an edible RA-rich plant grown in Taiwan. Our previous study found that an 80 % ethanol extract of T. khasianum Clarke leaves (80EETC) ameliorates gastric mucosal damage through its anti-inflammatory, antioxidant, and microbiota modulation abilities. However, the anti-obesity effect of 80EETC remains unclear. Therefore, the objective of this study was to explore the protective effects of low-dose 80EETC (125 mg/kg b.w., 80EETCL) or high-dose 80EETC (250 mg/kg b.w., 80EETCH) on obesity development through gut microbiota modulation in high-fat diet (HFD)-induced C57BL/6 mice. The results showed a high RA content (89.2 ± 7.4 mg/g) in 80EETC. 80EETC administration significantly decreased body weight, body fat ratio, serum lipid levels (TC, TG, and LDL-C), adipose tissue accumulation, malondialdehyde (MDA), and tumor necrosis factor-α (TNF-α) in HFD-fed mice. Furthermore, supplementation with 80EETC reduced the Firmicutes/Bacteroidetes ratio and enhanced the relative abundance of gut microbiota (p_Bacteroidetes, f_Lactobacillus, f_Muribaculaceae, f_Prevotellaceae, g_Lactobacillus, g_Prevotellaceae_NK3B31_group, g_Ruminococcaceae_UCG-013, and g_Ruminococcaceae_UCG-014), which negatively correlated with obesity-related factors such as body weight, energy intake, fat accumulation in adipose tissue, TC, TG, LDL, and MDA. In conclusion, RA-rich 80EETC had a protective effect against obesity development and it has potential in healthy food applications. Topics: Animals; Bacteroidetes; Body Weight; Diet, High-Fat; Dysbiosis; Mice; Mice, Inbred C57BL; Mice, Obese; Microbiota; Obesity; Plant Extracts; Rosmarinic Acid | 2023 |
Evaluation of rosmarinic acid against myocardial infarction in maternally separated rats.
Depression and coronary heart diseases are the common comorbid disorder affecting humans globally. The present study evaluated the effectiveness of rosmarinic acid (RA) against myocardial infarction (MI) in comorbid depression induced by maternal separation in rats. Maternal stress is one of the childhood crises that may be a potential risk factor for coronary heart disease in later part of life. As per protocol, 70-80% of pups were separated daily for 3 h between postnatal day 1 (PND1) and postnatal day 21 (PND21). Forced-swim test, sucrose preference test, and electrocardiography were performed during the experiment. Body weight was measured on PND0, PND35, and PND55. Orally rosmarinic acid (25 mg/kg and 50 mg/kg) and fluoxetine (10 mg/kg) was done from PND35 to PND55. On PND53 and PND54, isoproterenol (100 mg/kg, subcutaneously) was administered to induce myocardial infarction. On PND55, blood was collected and animals sacrificed, and plasma corticosterone, brain-derived neurotrophic factor, cardiac biomarkers, interleukine-10, and anti-oxidant parameters were measured. Rosmarinic acid and fluoxetine ameliorated the maternal separation-induced increase in immobility period, anhedonia, body weight, ST elevation, corticosterone, creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH). At the same time, both drugs elevated the tissue levels of BDNF, IL-10, glutathione, and superoxide dismutase activity. This study provides the first experimental evidence that maternal stress is an independent risk factor of cardiac abnormalities in rats. Moreover, maternal stress synergistically increases the severity of cardiac abnormalities induced by isoproterenol. Interestingly, fluoxetine and rosmarinic acid effectively ameliorated behavioral anomalies and myocardial infarction in maternally separated rats. Schematic representation of possible molecular mechanism of action of rosmarinic acid against MS-induced myocardial infarction. RA, rosmarinic acid; MS, maternal separation; PND, postnatal days; ISO, isoproterenol; BDNF, brain-derived neurotrophic factor; GSH, glutathione; SOD, superoxide dismutase; IL-10, interleukin-10; MI, myocardial infarction. Topics: Animals; Body Weight; Brain-Derived Neurotrophic Factor; Cinnamates; Corticosterone; Depsides; Fluoxetine; Glutathione; Interleukin-10; Isoproterenol; Maternal Deprivation; Myocardial Infarction; Myocardium; Oxidative Stress; Rats; Rats, Wistar; Rosmarinic Acid; Superoxide Dismutase | 2022 |
Protective roles and mechanisms of rosmarinic acid in cyclophosphamide-induced premature ovarian failure.
The aim of this study was to investigate the protective effect of rosmarinic acid (RA) in a premature ovarian failure (POF) mouse model and the potential mechanisms. The POF model was induced by a single intraperitoneal injection of 120 mg/kg cyclophosphamide (CP). Additionally, 40 mg/kg RA was administered for 7 days before CP injection. The concentration of sex hormones was determined by fluorescence immunohistochemistry. Histological analysis was performed after ovarian tissue sections were stained with hematoxylin and eosin. The expression of the NLRP3 inflammasome was examined by western blot analysis and polymerase chain reaction. The expression of apoptosis markers of cytochrome c and caspase-3 was also detected by western blot analysis and immunohistochemistry. The results showed that RA not only decreased the ovarian index in POF mice but also improved the abnormal secretion of reproductive hormones associated with POF. Treatment with RA suppressed the ovarian expression of the NLRP3 inflammasome and regulated the ovarian expression of apoptosis-related proteins. The results suggested that RA exhibited a protective effect against CP-induced POF potentially by suppressing apoptosis and the NLRP3 inflammasome. Topics: Animals; Apoptosis; Body Weight; Cinnamates; Cyclophosphamide; Depsides; Disease Models, Animal; Female; Humans; Injections, Intraperitoneal; Mice; Organ Size; Primary Ovarian Insufficiency; Rosmarinic Acid | 2020 |
Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats.
Rosmarinic acid (RA) is a natural pure compound from herbs belonging to the Lamiaceae family, such as rosemary, sage, basil, and mint. The antioxidant, angiotensin-converting enzyme inhibitory, and vasodilatory effects of RA have been revealed. Angiotensin II (ANG II) is a potent agent that generates hypertension and oxidative stress. Hypertension and skeletal muscle insulin resistance are strongly related. The aim of this study was to evaluate the effects of acute and chronic RA treatment on blood pressure and skeletal muscle glucose transport in ANG II-induced hypertensive rats.. Eight-week-old male Sprague Dawley rats were separated into SHAM and ANG II-infused (250 ng/kg/min) groups. ANG II rats were treated with or without acute or chronic RA at 10, 20, or 40 mg/kg. At the end of the experiment, body weight, liver and heart weights, oral glucose tolerance, skeletal muscle glucose transport activity, and signaling proteins were evaluated.. Both acute and chronic RA treatment decreased systolic, diastolic, and mean arterial blood pressure. Only acute RA at 40 mg/kg resulted in a reduction of fasting plasma glucose levels and an induction of skeletal muscle glucose transport activity. These effects might involve increased ERK activity in skeletal muscle. Meanwhile, chronic RA treatment with 10, 20, and 40 mg/kg prevented ANG II-induced hyperglycemia.. Both acute and chronic RA treatment attenuated ANG II-induced cardiometabolic abnormalities in rats. Therefore, RA would be an alternative strategy for improving skeletal muscle glucose transport and protecting against ANG II-induced hypertension and hyperglycemia. Topics: Angiotensin II; Animals; Blood Pressure; Body Weight; Cinnamates; Depsides; Glucose; Hypertension; Insulin; Male; Muscle, Skeletal; Organ Size; Rats; Rats, Sprague-Dawley; Rosmarinic Acid; Signal Transduction | 2019 |
Beneficial effects of rosmarinic acid against alcohol-induced hepatotoxicity in rats.
Alcohol is a severe hepatotoxicant that causes a variety of liver disorders. Rosmarinic acid (RA), a natural phenol, shows some biological activities, including antioxidant and anti-inflammatory effects. We investigated the effects of RA (10 mg/kg) against ethanol-induced oxidative damage and hepatotoxicity in rats. Animals received ethanol (4 g/kg, i.g.) and (or) RA (10 mg/kg, i.g.) daily for 4 weeks. At the end of the treatment period, rats were weighed and use for biochemical, molecular, and histopathological examinations. Ethanol increased hepatic lipid peroxidation (P < 0.001) and decreased hepatic levels of reduced glutathione (P < 0.01), catalase (P < 0.05), and superoxide dismutase (P < 0.001) compared with control group. RA prevented the prooxidant and antioxidant imbalance induced by ethanol in liver. Furthermore, RA ameliorated the increased liver mass, serum levels of ALT, AST, LDH, TNF-α, and IL-6 in ethanol group. Necrosis and infiltration of inflammatory cells in liver parenchyma were attenuated by RA treatment. Our findings showed that RA prevents ethanol-induced oxidant/antioxidant imbalance and liver injury in an experimental model of ethanol-induced hepatotoxicity. Therefore, RA may be a good candidate to protect against ethanol-induced hepatotoxicity; this deserves consideration and further examination. Topics: Animals; Biomarkers; Body Weight; Catalase; Cinnamates; Cytokines; Depsides; Ethanol; Glutathione; Inflammation Mediators; Interleukin-6; Lipid Peroxidation; Liver; Male; Malondialdehyde; Organ Size; Paraffin Embedding; Rats, Wistar; Rosmarinic Acid; Superoxide Dismutase; Tumor Necrosis Factor-alpha | 2018 |
Anti-inflammatory effects of rosmarinic acid-4-O-β-D-glucoside in reducing acute lung injury in mice infected with influenza virus.
Rosmarinic acid-4-O-β-D-glucoside (RAG) is a dicaffeoyl phenolic compound isolated from Sarcandra glabra (Thunb.) Nakai. Preliminary studies show that RAG has significant anti-inflammatory properties and can alleviate ear swelling in mice and the paw swelling in rats. Here, the anti-influenza effects of RAG were investigated in mice infected with A/FM/1/47 H1N1 virus. The survival rate and body weight were observed, the lung edema, virus copies, inflammatory cytokines (including IL-4, IL-5, TNF-α and IFN-γ) and oxidative damage indexes (including SOD, MDA, NO, and CAT) were measured. Moreover, immune cell recruitment in alveoli was measured with white blood cells and differential counts. Therapeutic RAG concentrations substantially improve the symptoms, mitigate body weight loss and alleviate lung edema induced by virus, thus improve survival protection effects. Furthermore, RAG was shown to regulate influenza virus-induced inflammatory cytokine expression, specifically by downregulating the Th1 cell cytokines IFN-γ, TNF-α and upregulating the Th2 cell cytokines IL-4, IL-5. Cell migration and infiltration were also diminished after RAG administration. Topics: Acute Lung Injury; Animals; Anti-Inflammatory Agents, Non-Steroidal; Body Weight; Cinnamates; Cytokines; Depsides; Disease Models, Animal; Glucosides; Lung; Mice; Orthomyxoviridae Infections; Rosmarinic Acid; Survival Analysis; Viral Load | 2017 |
Biochemical and molecular mechanisms underlying the chemopreventive efficacy of rosmarinic acid in a rat colon cancer.
To shed light on colon cancer chemoprevention, natural phytochemicals attract researchers by virtue of their beneficial biological effects. The chemopreventive potential of rosmarinic acid (RA) was tested by using the colon carcinogen, 1,2-dimethylhydrazine (DMH) by evaluating the Aberrant crypt foci (ACF), tumour incidence, lipid peroxidative byproducts, phase I & II drug metabolizing enzymes, cell proliferative and apoptotic proteins. Rats were divided into six groups and received modified pellet diet. Group 1 served as control rats, group 2 rats received RA (5mg/kg b.w. p.o.), rats in groups 3-6 received DMH (20mg/kg b.w., s.c.) for the first fifteen weeks. In addition to DMH, groups 4-6 received RA at the dose of 5mg/kg b.w. during initiation, post initiation stages and also for the entire study period. DMH treated rats showed an increase in the development of ACF, tumour formation and multiplicity and decrease in lipid peroxidative byproducts. Moreover, it modulates xenobiotic enzymes and reduces the expressions of proapoptotic proteins; increases expressions of anti apoptotic proteins at the end of the study. Supplementation with RA to carcinogen treated rats protected them from the above deleterious effects caused by DMH and thus RA may be used as a potent chemopreventive agent. Topics: Animals; Anticarcinogenic Agents; Apoptosis; Body Weight; Carcinogenesis; Carcinogens; Cinnamates; Colonic Neoplasms; Depsides; Feces; Gene Expression Regulation, Neoplastic; Intestinal Mucosa; Lipid Peroxidation; Rats; RNA, Messenger; Rosmarinic Acid; Tumor Suppressor Protein p53; Xenobiotics | 2016 |
Rosmarinic acid stimulates liver regeneration through the mTOR pathway.
Rosemary (Rosmarinus offcinsalis L) has a liver protection function under various conditions of liver damage. Rosmarinic acid, one of the pharmacological constituents of rosemary, exhibited protective effects against organ injury, including acute liver injury.. We hypothesize that RA stimulates liver regeneration.. In the present study, we investigated the effects and mechanism of RA administration on liver regeneration using partial hepatectomy (PH), a well-validated liver regeneration model in mice.. We use a 2/3 partial hepatectomy (PH) model to induce liver regeneration. RA was administered prior to and simultaneously with PH. The regeneration process was estimated by the index of the liver to body weight (ILBW) and the expression of proliferating cell nuclear antigen (PCNA) and liver transaminases.. The administration of rosmarinic acid stimulated hepatocyte proliferation based on activation of the mTOR/S6K pathway. Rosmarinic acid treatment also rescued impaired liver function due to PH.. These data demonstrate that RA is potentially useful to promote liver regeneration. Topics: Animals; Body Weight; Cell Proliferation; Cinnamates; Depsides; Hepatectomy; Hepatocytes; Liver; Liver Function Tests; Liver Regeneration; Male; Mice, Inbred C57BL; Proliferating Cell Nuclear Antigen; Rosmarinic Acid; TOR Serine-Threonine Kinases | 2016 |
Effect of rosmarinic acid on experimental diabetic nephropathy.
Connective tissue growth factor (CTGF) plays a pathogenic role in diabetic nephropathy (DN). Rosmarinic acid (RA) is a naturally occurring phenolic acid. This study was conducted to investigate the efficacy of RA on DN and to elucidate the potential mechanism. High glucose (HG)-stimulated cultured human renal proximal tubular epithelial cells (HK-2) analysed CTGF expression by western blotting, and it was investigated whether extracellular signal-regulated kinase (ERK) signalling pathway was involved. Using streptozotocin (STZ)-induced rat animal models, diabetic rats were randomized to receive intragastric (i.g.) doses of RA. Renal tissue, blood and urine samples were collected to determine biochemical index and analyse protein expression. In vitro study, RA reduced CTGF excretion in HG-induced HK-2 cells through the ERK signalling pathway. In an in vivo study, I.g. of RA 7.5 or 15 mg/kg significantly ameliorated renal function and increased body-weight. Meanwhile, RA reduced renal CTGF expression by immunohistochemical staining and reduced serum levels of CTGF. Besides, there were no significant differences in glycaemia levels between the RA groups compared with the STZ-treated group. Furthermore, RA ameliorated renal pathology. These results suggest that RA exerts an early renal protective role to DN. Inhibition of CTGF may be a potential target in DN therapy, which highlights the possibility of using RA in the treatment of DN. Topics: Animals; Body Weight; Cells, Cultured; Cinnamates; Connective Tissue Growth Factor; Depsides; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Dose-Response Relationship, Drug; Epithelial Cells; Humans; Kidney Tubules, Proximal; Male; Pilot Projects; Random Allocation; Rats; Rats, Sprague-Dawley; Rosmarinic Acid; Streptozocin | 2012 |
Administration of rosmarinic acid reduces cardiopathology and blood pressure through inhibition of p22phox NADPH oxidase in fructose-fed hypertensive rats.
Rosmarinic acid (RA), a caffeic acid ester, has insulin-sensitizing and antioxidant effects in high fructose-fed model of insulin resistance (IR). This study investigated whether RA supplementation prevents cardiac abnormalities and hypertension in fructose-fed rats (FFR). Rats fed with fructose diet (60 g/100 g) for 60 days exhibited metabolic abnormalities and rise in plasma and cardiac lipids and whole body IR. The levels of cardiac antioxidants and plasma ferric reducing antioxidant power were significantly reduced in FFR concomitant with increased levels of lipid peroxidation and protein oxidation products. A significant rise in troponin T, creatine kinase-MB, aspartate transaminase, and lactate dehydrogenase in plasma of FFR was noted. RA supplementation to FFR (10 mg/kg from the 16th day) significantly improved insulin sensitivity, reduced lipid levels, oxidative damage, and the expression of p22phox subunit of nicotinamide adenine dinucleotide phosphate reduced oxidase, and prevented cardiac hypertrophy. Fructose-induced rise in blood pressure was also lowered by RA through decrease in endothelin-1 and angiotensin-converting enzyme activity and increase in nitric oxide levels. Histology revealed a reduction in myocardial damage in RA-supplemented FFR. These findings suggest that RA acts as a vasoactive substance and a cardioprotector through its antioxidant property. Thus, RA may be useful in reducing the cardiovascular risk associated with IR. Topics: Animals; Antioxidants; Aspartate Aminotransferases; Blood Glucose; Blood Pressure; Body Weight; Cinnamates; Creatine Kinase, MB Form; Depsides; Dietary Carbohydrates; Endothelin-1; Fructose; Gene Expression; Heart; Hyperinsulinism; Hypertension; Insulin; Insulin Resistance; Kallikreins; L-Lactate Dehydrogenase; Lipid Metabolism; Lipids; Male; Myocardium; NADPH Oxidases; Nitrates; Nitric Oxide Synthase Type III; Organ Size; Oxidative Stress; Peptidyl-Dipeptidase A; Rats; Rats, Wistar; Rosmarinic Acid; Troponin C | 2011 |
Effect of rosmarinic acid in motor dysfunction and life span in a mouse model of familial amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis (ALS) is a late-onset progressive neurodegenerative disease affecting motor neurons. About 2% of patients with the disease are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1). The purpose of this study is to assess the effect of rosemary extract and its major constituents, rosmarinic acid (RA) and carnosic acid (CA), in human SOD1 G93A transgenic mice, which are well-established mouse models for ALS. The present study demonstrates that intraperitoneal administration of rosemary extract or RA from the presymptomatic stage significantly delayed motor dysfunction in paw grip endurance tests, attenuated the degeneration of motor neurons, and extended the life span of ALS model mice. In addition, RA administration significantly improved the clinical score and suppressed body weight loss compared with a vehicle-treated group. In conclusion, this study provides the first report that rosemary extract and, especially, RA have preventive effects in the mouse model of ALS. Topics: Aging; Amyotrophic Lateral Sclerosis; Animals; Antioxidants; Body Weight; Cinnamates; Depsides; Disease Models, Animal; Humans; Longevity; Mice; Mice, Transgenic; Motor Activity; Motor Neurons; Movement Disorders; Mutation; Phytotherapy; Psychomotor Performance; Rosmarinic Acid; Rosmarinus; Spinal Cord; Superoxide Dismutase | 2010 |
Effects of a water-soluble extract of rosemary and its purified component rosmarinic acid on xenobiotic-metabolizing enzymes in rat liver.
The effects of a water-soluble extract (WSE) of rosemary and its purified antioxidant rosmarinic acid (RA) on xenobiotic metabolizing enzymes (XME) were studied in rat liver after dietary administration. The modulation of phase I enzymes such as cytochrome P450 (CYP) 1A, 2B, 2E1, 3A, and phase II enzymes such as glutathione S-transferase (GST), quinone reductase (QR) and UDP-glucuronosyltransferase (UGT) was evaluated by measuring enzyme activities with specific substrates. Protein levels of CYPs and rGST A1/A2, A3/A5, M1, M2 and P1 were measured using antibodies in Western blots. Caffeic acid was also studied because it results from RA biotransformation in rat after oral administration. Male SPF Wistar rats received the different compounds at 0.5% (w/w) incorporated into their diet for 2 weeks. WSE, containing RA, flavones and monoterpenes enhanced CYP 1A1, 2B1/2, 2E1 and GST (especially rGST A3/A5, M1 and M2), QR and UGT. On the contrary, no modification of XME was observed in response to RA or CA (except for a slight increase of UGT activity after CA treatment). The induction of XME by WSE could be attributed to flavones, monoterpenes or an additive effect of all components. Topics: Animals; Biomarkers; Body Weight; Chromatography, High Pressure Liquid; Cinnamates; Cytosol; Depsides; Diet; Flavonoids; Immunoblotting; Lamiaceae; Liver; Male; Microsomes, Liver; Organ Size; Plant Extracts; Rats; Rats, Wistar; Rosmarinic Acid; Spectrophotometry, Ultraviolet; Stimulation, Chemical; Terpenes; Xenobiotics | 2001 |