Ameliorative potential of resveratrol on proinflammatory cytokines, hyperglycemia mediated oxidative stress, and pancreatic β‐cell dysfunction in streptozotocin‐nicotinamide‐induced diabetic rats

Periyasamy, Palsamy; Subramanian, S.

doi:10.1002/jcp.22138

Cited by 176 publications

(137 citation statements)

References 81 publications

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“…RV significantly reduced the elevated levels of TBARS and activities of catalase and glutathione-S transferase in the hepatic tissue compared to the methotrexate-treated group. RV (5 mg/kg bw for 30 days) found a reduction of the levels of blood glucose, glycosylated hemoglobin, TNF-alpha, interleukin-1-beta, interleukin-6, NF-kappaB p65 unit and NO with increase in plasma insulin in diabetic rats (29). Bi et al (30) found that RV treatment significantly inhibited the release of TNF-alpha and nitrite oxide induced by lipopolysaccharide (LPS) in rat cortical microglia and a mouse microglial cell line N9 in vitro.…”

Section: Discussionmentioning

confidence: 88%

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Aydın¹,

Şahin²,

Bacanlı³

et al. 2016

Balkan Med J

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Background:The increases of free radicals have been proposed to be involved in the pathogenesis of sepsis, which leads to multiple-organ dysfunction syndromes. The uses of antioxidants as a complementary tool in the medical care of oxidative stress-related diseases have attracted attention of researchers. Resveratrol (RV) has suggested being antioxidant, anti-proliferative, and anti-inflammatory effects in various experimental models and clinical settings. Aims: This study was undertaken to evaluate the protective effects of RV on oxidative DNA damage induced by sepsis in the liver and kidney tissues of Wistar albino rats. Study Design: Animal experimentation. Methods: Four experimental groups consisting of eight animals for each was created using a total of thirty-two male Wistar albino rats. Sham group was given 0.5 mL of saline intra-peritoneal (ip) only following laparatomy. Sepsis group was given 0.5 mL saline ip only following the induction of sepsis. RV-treated group was given a dose of 100 mg/kg ip RV in 0.5 mL saline following laparatomy. RVtreated sepsis group was given 100 mg/kg ip RV in 0.5 mL saline following the induction of sepsis. A model of sepsis was created by cecal ligation and puncture technique. In the liver and kidney tissues, oxidative stress parameters (malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPX)) and a proinflammatory cytokine (tumor necrosis factor alpha (TNF-alpha)), were evaluated spectrophotometrically and DNA damage was determined by the alkaline single cell gel electrophoresis (comet assay) technique using formamidopyrimidine DNA glycosylase protein. Results:In the RV-treated sepsis group, the levels of MDA and TNF-alpha were lower and GSH levels, SOD and GPX activities were higher than in the septic rats (p<0.05). RV treatment significantly reduced the sepsis-induced oxidative DNA damage in the liver and kidney cells (p<0.05). Conclusion: It is suggested that RV treatment might reduce the sepsis-induced oxidative DNA damages in sepsis-related diseases; however, there is a need for more studies to clear up the protective mechanisms of RV against sepsis.

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Section: Discussionmentioning

confidence: 88%

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Aydın¹,

Şahin²,

Bacanlı³

et al. 2016

Balkan Med J

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“…Along with the generation of ROS, relatively longterm exposure of MIN6 cells to insulin did appear to increase significantly the expressions of the antioxidant enzymes Cat and Gpx, as occurs with some other inducers of cellular stress (Tiedge et al 1997, Laybutt et al 2002, Palsamy & Subramanian 2010, Chetboun et al 2012, Bhakkiyalakshmi et al 2014, Tersey et al 2014, Vasu et al 2014. In contrast, the expressions of Sod1 and Sod2 were only slightly and not significantly increased by 24 and 48 h insulin exposure.…”

Section: :3mentioning

confidence: 79%

Prolonged insulin treatment sensitizes apoptosis pathways in pancreatic β cells

Bucris

Beck

Boura‐Halfon

et al. 2016

Journal of Endocrinology

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Insulin resistance results from impaired insulin signaling in target tissues that leads to increased levels of insulin required to control plasma glucose levels. The cycle of hyperglycemia and hyperinsulinemia eventually leads to pancreatic β cell deterioration and death by a mechanism that is yet unclear. Insulin induces ROS formation in several cell types. Furthermore, death of pancreatic β cells induced by oxidative stress could be potentiated by insulin. Here, we investigated the mechanism underlying this phenomenon. Experiments were done on pancreatic β cell lines (Min-6, RINm, INS-1), isolated mouse and human islets, and on cell lines derived from nonpancreatic sources. Insulin (100 nM) for 24 h selectively increased the production of ROS in pancreatic β cells and isolated pancreatic islets, but only slightly affected the expression of antioxidant enzymes. This was accompanied by a time-and dose-dependent decrease in cellular reducing power of pancreatic β cells induced by insulin and altered expression of several ER stress response elements including a significant increase in Trb3 and a slight increase in iNos. The effect on iNos did not increase NO levels. Insulin also potentiated the decrease in cellular reducing power induced by H 2 O 2 but not cytokines. Insulin decreased the expression of MCL-1, an antiapoptotic protein of the BCL family, and induced a modest yet significant increase in caspase 3/7 activity. In accord with these findings, inhibition of caspase activity eliminated the ability of insulin to increase cell death. We conclude that prolonged elevated levels of insulin may prime apoptosis and cell death-inducing mechanisms as a result of oxidative stress in pancreatic β cells.

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“…Moreover, GSH, a co-substrate for glutathione peroxidase activity, is another major intra-and extracellular antioxidant molecule and acts as a direct free radical scavenger by conversion to GSSG [13]. GSSG to GSH ratio is a good marker for estimation of redox status [12,22].…”

Section: Diabetic Heart and Oxidative Stressmentioning

confidence: 99%

Chronic resveratrol administration improves diabetic cardiomyopathy in part by reducing oxidative stress

2014

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8-isoprostane, 6.03 ± 0.87 vs. 8.49 ± 0.52 µmol, p < 0.05 for nitrite/nitrate, and 0.44 ± 0.03 vs. 0.59 ± 0.04, p < 0.05 for oxidized/reduced glutathione ratio), nuclear factor kappa B activity (0.37 ± 0.09 vs. 0.60 ± 0.11, p < 0.05) and apoptosis rate (0.98 ± 0.28 vs. 1.63 ± 0.16, p < 0.05). Moreover, it improved left ventricular developed pressure (72.46 ± 8.16 vs. 52.01 ± 11.32 mm Hg, p < 0.05) and coronary flow (14.08 ± 1.09 vs. 11.75 ± 1.43 mL/ /min × g, p < 0.05). Conclusions: These beneficial cardioprotective observations suggest that treatment with resveratrol can potentially delay or attenuate the progression of diabetes-related cardiac complications. (Cardiol J 2014; 21, 1: 39-46)

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Ameliorative potential of resveratrol on proinflammatory cytokines, hyperglycemia mediated oxidative stress, and pancreatic β‐cell dysfunction in streptozotocin‐nicotinamide‐induced diabetic rats

Cited by 176 publications

References 81 publications

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Prolonged insulin treatment sensitizes apoptosis pathways in pancreatic β cells

Chronic resveratrol administration improves diabetic cardiomyopathy in part by reducing oxidative stress

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