Protective effects of resveratrol against streptozotocin-induced diabetes in rats by modulation of visfatin/sirtuin-1 pathway and glucose transporters

2015 ◽  
Vol 66 (3) ◽  
pp. 314-320 ◽  
Author(s):  
Hasan Gencoglu ◽  
Mehmet Tuzcu ◽  
Armagan Hayirli ◽  
Kazim Sahin
Keyword(s):  
Glucose Transporters ◽  
Sirtuin 1 ◽  
Protective Effects ◽  
Streptozotocin Induced Diabetes

Protective efficacy of carnosic acid against hydrogen peroxide induced oxidative injury in HepG2 cells through the SIRT1 pathway

2015 ◽  
Vol 93 (8) ◽  
pp. 625-631 ◽  
Author(s):  
Yan Hu ◽  
Ning Zhang ◽  
Qing Fan ◽  
Musen Lin ◽  
Ce Zhang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Caspase 3 ◽  
Protective Efficacy ◽  
B Cell Lymphoma ◽  
Sirtuin 1 ◽  
Carnosic Acid ◽  
Protective Effects ◽  
Hepatocyte Damage

Carnosic acid (CA), found in rosemary, has been reported to have antioxidant and antiadipogenic properties. Here, we investigate the molecular mechanism by which CA inhibits hydrogen peroxide (H2O2)-induced injury in HepG2 cells. Cells were pretreated with 2.5–10 μmol/L CA for 2 h and then exposed to 3 mmol/L H2O2 for an additional 4 h. CA dose-dependently increased cell viability and decreased lactate dehydrogenase activities. Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3. Importantly, sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, was significantly increased by CA. Considering the above results, we hypothesized that SIRT1 may play important roles in the protective effects of CA in injury induced by H2O2. As expected, SIRT1 suppression by Ex527 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide) and siRNA-mediated SIRT1 silencing (si-SIRT1) significantly aggravated the H2O2-induced increased level of cleaved caspase-3 but greatly reduced the decreased expression of MnSOD and Bcl-xL. Furthermore, the positive regulatory effect of CA was inhibited by si-SIRT1. Collectively, the present study indicated that CA can alleviate H2O2-induced hepatocyte damage through the SIRT1 pathway.

scholarly journals Antihyperlipidemic and Biochemical Activities of Mcy Protein in Streptozotocin Induced Diabetic Rats

2015 ◽  
Vol 35 (4) ◽  
pp. 1326-1334 ◽  
Author(s):  
Saritha Marella ◽  
Dilip Rajasekhar Maddirela ◽  
Kameswara Rao Badri ◽  
Malaka Venkateshwarulu Jyothi Kumar ◽  
Apparao Chippada
Keyword(s):  
Blood Glucose ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
Albino Rats ◽  
Protective Effects ◽  
Tissue Lipid ◽  
Lipid Levels ◽  
Liver And Kidney ◽  
Streptozotocin Induced Diabetes ◽  
Wistar Albino Rats

Background: This study was aimed to evaluate the protective effects of a novel anti-hyperglycemic “Mcy protein” isolated from the fruits of Momordica cymbalaria in streptozotocin induced- diabetes rat model. Materials and Methods: Wild type and Streptozotocin induced diabetic male wistar albino rats were either treated with single intraperitoneal injection of 2.5 mg Mcy protein/kg body weight or acetate buffer daily for 30 days. Fasting blood glucose and, serum and tissue lipid levels were measured along with biochemical analysis for hepatic and renal function tests. Results: Mcy protein significantly reduced the fasting blood glucose and, serum as well as tissue lipid levels (p<0.05), besides normalizing the levels of liver and kidney function markers in the treated diabetic rats when compared to the diabetic controls. Our studies also showed the pancreatic islet regeneration in Mcy treated rats. Conclusion: Mcy protein can alleviate hyperlipidemia and help manage diabetes by stimulating insulin secretion without evident toxic effects on liver and kidney.

scholarly journals Partially Hydrolyzed Guar Gum Attenuates d-Galactose-Induced Oxidative Stress and Restores Gut Microbiota in Rats

2019 ◽  
Vol 20 (19) ◽  
pp. 4861 ◽  
Author(s):  
Xiaoyan Liu ◽  
Chenxuan Wu ◽  
Dong Han ◽  
Jun Liu ◽  
Haijie Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Guar Gum ◽  
Telomerase Activity ◽  
Sirtuin 1 ◽  
Protective Effects ◽  
Rat Serum ◽  
Oxidative Damages ◽  
Partially Hydrolyzed Guar Gum

Partially hydrolyzed guar gum (PHGG) has received considerable attention for its various bioactive functions. The injection of d-galactose can cause aging-related injury which is usually resulted from oxidative stress on tissues and cells. In this study, d-galactose (200 mg/kg/day) was injected into rats, and the protective effects of PHGG (500, 1000, and 1500 mg/kg/day) against oxidative damages, as well as its probiotic functions, were analyzed. The results showed that PHGG treatment at a concentration of 1500 mg/kg/day greatly reduced the levels of lactic acid, nitric oxide, inducible nitric oxide synthase, advanced glycation end products, and increased the telomerase activity, by 7.60%, 9.25%, 12.28%, 14.58%, and 9.01%, respectively. Moreover, PHGG significantly elevated the activities of antioxidant enzymes and decreased the content of malondialdehyde in rat serum and brain. The oxidative damage was also significantly alleviated in the liver and hippocampus and the expressions of brain-derived neurotrophic factor and choline acetyltransferase also increased. Furthermore, PHGG treatment could significantly regulated the expression of sirtuin 1, forkhead box O1, and tumor protein p53 in the hippocampus. It also increased the levels of organic acids and improved the composition of intestinal microbiota. These findings demonstrated that PHGG treatment could effectively alleviate the oxidative damage and dysbacteriosis.

scholarly journals Comparison of the Effect of Melatonin Treatment before and after Brain Ischemic Injury in the Inflammatory and Apoptotic Response in Aged Rats

2018 ◽  
Vol 19 (7) ◽  
pp. 2097 ◽  
Author(s):  
Lisa Rancan ◽  
Sergio Paredes ◽  
Cruz García ◽  
Pablo González ◽  
Cruz Rodríguez-Bobada ◽  
...  
Keyword(s):  
B Cell Lymphoma ◽  
Free Radical Scavenger ◽  
Sirtuin 1 ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Ischemic Lesion ◽  
Melatonin Administration ◽  
Brain Ischemic Injury ◽  
Before And After ◽  
Factor Α

Aging is associated with an increase in stroke risk. Melatonin, a potent free radical scavenger and broad spectrum antioxidant, has been shown to counteract inflammation and apoptosis in brain injury. However, little is known on the possible protective effects of melatonin in aged individuals affected by brain ischemia. Also, using melatonin before or after an ischemic stroke may result in significantly different molecular outcomes. The objective of the present study was to compare the effects of pre-ischemia vs. post-ischemia melatonin administration in an ischemic lesion in the cortex and hippocampus of senescent Wistar rats. An obstruction of the middle cerebral artery (MCA) to 18-month-old animals was performed. In general, animals treated with melatonin from 24 h prior to surgery until 7 days after the surgical procedure (PrevT) experienced a significant decrease in the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), glial fibrillary acidic protein (GFAP), Bcl-2-associated death promoter (BAD), and Bcl-2-associated X protein (BAX) in both cortex and hippocampus, while hippocampal levels of sirtuin 1 (SIRT1) and B-cell lymphoma 2 (Bcl-2) increased. Treatment of animals with melatonin only after surgery (AT) resulted in similar effects, but to a lesser extent than in the PrevT group. In any case, melatonin acted as a valuable therapeutic agent protecting aged animals from the harmful effects of cerebral infarction.

scholarly journals The Protective Effects of CD39 Overexpression in Multiple Low-Dose Streptozotocin-Induced Diabetes in Mice

Diabetes ◽  
2013 ◽  
Vol 62 (6) ◽  
pp. 2026-2035 ◽  
Author(s):  
J. S. J. Chia ◽  
J. L. McRae ◽  
H. E. Thomas ◽  
S. Fynch ◽  
L. Elkerbout ◽  
...  
Keyword(s):  
Low Dose ◽  
Protective Effects ◽  
Diabetes In Mice ◽  
Streptozotocin Induced Diabetes

scholarly journals Alanyl-glutamine improves pancreatic β-cell function following ex vivo inflammatory challenge

2014 ◽  
Vol 224 (3) ◽  
pp. 261-271 ◽  
Author(s):  
Vinicius Fernandes Cruzat ◽  
Kevin Noel Keane ◽  
Anita Lavarda Scheinpflug ◽  
Robson Cordeiro ◽  
Mario J Soares ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Function ◽  
Ex Vivo ◽  
Sirtuin 1 ◽  
Protective Effects ◽  
Pancreatic Β Cell ◽  
Cell Integrity ◽  
Cell Protection ◽  
Β Cells ◽  
Β Cell

Obesity-associated diabetes and concomitant inflammation may compromise pancreatic β-cell integrity and function. l-glutamine and l-alanine are potent insulin secretagogues, with antioxidant and cytoprotective properties. Herein, we studied whether the dipeptide l-alanyl-l-glutamine (Ala-Gln) could exert protective effects via sirtuin 1/HUR (SIRT1/HUR) signalling in β-cells, against detrimental responses following ex vivo stimulation with inflammatory mediators derived from macrophages (IMMs). The macrophages were derived from blood obtained from obese subjects. Macrophages were exposed (or not) to lipopolysaccharide (LPS) to generate a pro-inflammatory cytokine cocktail. The cytokine profile was determined following analysis by flow cytometry. Insulin-secreting BRIN–BD11 β-cells were exposed to IMMs and then cultured with or without Ala-Gln for 24 h. Chronic insulin secretion, the l-glutamine–glutathione (GSH) axis, and the level of insulin receptor β (IR-β), heat shock protein 70 (HSP70), SIRT1/HUR, CCAAT-enhancer-binding protein homologous protein (CHOP) and cytochrome c oxidase IV (COX IV) were evaluated. Concentrations of cytokines, including interleukin 1β (IL1β), IL6, IL10 and tumour necrosis factor alpha (TNFα) in the IMMs, were higher following exposure to LPS. Subsequently, when β-cells were exposed to IMMs, chronic insulin secretion, and IR-β and COX IV levels were decreased, but these effects were partially or fully attenuated by the addition of Ala-Gln. The glutamine–GSH axis and HSP70 levels, which were compromised by IMMs, were also restored by Ala-Gln, possibly due to protection of SIRT1/HUR levels, and a reduction of CHOP expression. Using an ex vivo inflammatory approach, we have demonstrated Ala-Gln-dependent β-cell protection mediated by coordinated effects on the glutamine–GSH axis, and the HSP pathway, maintenance of mitochondrial metabolism and stimulus–secretion coupling essential for insulin release.

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