Protective effects of epicatechin against the toxic effects of streptozotocin on rat pancreatic islets: in vivo and in vitro.
ABSTRACT Green tea catechins have diverse pharmacological effects such as anticarcinogenic and antioxidant activities.
To study the protective effects of green tea (-)-epicatechin (EC) against the toxic effects of streptozotocin (STZ), a selective beta cell toxin, on pancreatic islets in vivo and in vitro.
Rats were randomly divided into four groups: control, EC (30 mg/kg)-treated, STZ (60 mg/kg)-treated, and EC plus STZ (same doses; EC+STZ)-treated rats. EC was administered twice a day for 6 days, and a single injection of STZ was used. In EC+STZ-treated rats, EC was administered 6 hours prior to STZ since posttreatment with EC had no beneficial effects on fully developed diabetes in our unpublished study. Insulin and insulin mRNA were detected by immunohistochemical analysis and in situ hybridization, respectively, and physiologic parameters including blood glucose concentration were measured daily. Following isolation of the islets, insulin release, nitrite levels, and islet morphology were observed in the four groups: control, EC (0.8 mM)-treated, STZ (5 mM)-treated, and EC+STZ (same doses)-treated islets.
In EC+STZ-treated rats, hyperglycemia and weight loss were not observed and islet morphology was well preserved compared with STZ-treated rats. Compared with STZ treatment alone, insulin release was increased and nitrite production was decreased in EC+STZ-treated islets.
EC appears to be helpful in protecting pancreatic islets against exposure to STZ in both in vivo and in vitro systems.
- SourceAvailable from: Adnan Kausar
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- "PYC administration can counteract cytokine-induced activation of NFκB (Fujimoto et al. 2005). Other possible mechanisms of action by which PYC is showing antidiabetic potential presence of its active constituents, each acts with different mechanism, are: oligomeric procyanidin (inhibits alpha-glucosidase activity ), monomeric epicatechin (induces pancreatic beta cell regeneration ), and catechin (inhibits intestinal glucose absorption) (Shimizu et al. 2000; Kim et al. 2003; Schafer and Hogger 2007). "
ABSTRACT: A number of experimental and clinical findings have consistently demonstrated the protective effects of Pycnogenol® (PYC) in the management of diabetes. However, the protective mechanism by which PYC provides protection in a model type I diabetes has not been studied. This study examines the beneficial effect of PYC on hyperglycemia, inflammatory markers, and oxidative damage in diabetic rats. We also evaluated the possible mechanism of action of PYC which might be that it stimulates beta islet expression, which has been implicated in the process of insulin secretion and diabetes management. Diabetes was induced in rats by an intraperitoneal injection of streptozotocin (STZ; 60 mg/kg body weight) followed by free access to 5 % glucose for the next 24 h. Four days after STZ injection, rats were supplemented with PYC (10 mg/kg body weight) for 4 weeks. At the end of the experiment, blood was drawn, and rats were then sacrificed, and their livers and pancreases were dissected for biochemical and histological assays. The level of fasting blood glucose and glycosylated hemoglobin significantly increased but amylase, insulin, and hepatic glycogen level decreased in the STZ group. PYC significantly augmented these effects in STZ + PYC group. The STZ group showed elevated level of nitric oxide, tumor necrosis factor-α, and interleukin-1beta in serum which were decreased by PYC treatment. Moreover, PYC significantly ameliorated increased thiobarbituric reactive substances, protein carbonyl, and decreased levels of glutathione, glutathione-s-transferase, and catalase activity in the liver and pancreas of the STZ rats. Histopathological and immunohistochemical examination also revealed a remarkable protective effect of PYC. The study suggests that PYC is effective in reducing diabetic-related complications in a type I model of diabetes and might be beneficial for the treatment of diabetic patients.Protoplasma 06/2012; 250(1). DOI:10.1007/s00709-012-0418-2 · 3.17 Impact Factor
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- "Another study has reported that EC can also reduce the toxicity of STZ in rat pancreatic islets . Rats were randomly divided into four groups: control, EC (30 mg/kg)-treated, STZ (60 mg/kg)-treated, and EC (30 mg/kg) plus STZ (60 mg/kg)-treated. "
ABSTRACT: Green tea (Camellia sinensis, Theaceace) is the second most popular beverage in the world and has been extensively studied for its putative disease preventive effects. Green tea is characterized by the presence of a high concentrations of polyphenolic compounds known as catechins, with (-)-epigallocatechin-3-gallate (EGCG) being the most abundant and most well-studied. Metabolic syndrome (MetS) is a complex condition that is defined by the presence of elevated waist circumference, dysglycemia, elevated blood pressure, decrease serum high-density lipoprotein-associated cholesterol, and increased serum triglycerides. Studies in both in vitro and laboratory animal models have examined the preventive effects of green tea and EGCG against the symptoms of MetS. Overall, the results of these studies have been promising and demonstrate that green tea and EGCG have preventive effects in both genetic and dietary models of obesity, insulin resistance, hypertension, and hypercholesterolemia. Various mechanisms have been proposed based on these studies and include: modulation of dietary fat absorption and metabolism, increased glucose utilization, decreased de novo lipogenesis, enhanced vascular responsiveness, and antioxidative effects. In the present review, we discuss the current state of the science with regard to laboratory studies on green tea and MetS. We attempt to critically evaluate the available data and point out areas for future research. Although there is a considerable amount of data available, questions remain in terms of the primary mechanism(s) of action, the dose-response relationships involved, and the best way to translate the results to human intervention studies.Pharmacological Research 12/2010; 64(2):146-54. DOI:10.1016/j.phrs.2010.12.013 · 3.98 Impact Factor
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- "As a consequence of insulin resistance the pancreas continues to produce insulin causing hyperinsulinemia (Bitar et al., 2005). The significant improvement (p ≤ 0.05) of radiationinduced hyperglycemia and hyperinsulinemia in GSEtreated irradiated rats, compared with their corresponding values in irradiated rats (Table 3) is consistent with glucose-lowering activity of GSE (Kim et al., 2003) and its effect on insulin resistance (Al-Awwadi et al., 2005). "
ABSTRACT: Whole body exposure to ionizing radiation induces the formation of reactive oxygen species (ROS) in different tissues provoking oxidative damage, organ dysfunction and metabolic disturbances. The present study was designed to determine the possible protective effect of grape seed extract (GSE), rich in proanthocyanidins against gamma-radiation-induced oxidative stress in heart and pancreas tissues associated with serum metabolic disturbances. Irradiated rats were whole body exposed to 5 Gy gamma-radiation. GSE-treated irradiated rats received 100 mg GSE/kg/day, by gavage, for 14 days before irradiation. The animals were killed on days 1, 14 and 28 after irradiation. Significant decreases of SOD, CAT and GSH-Px activities associated with significant increases of TBARS levels were recorded in both tissues after irradiation. GSE administration pre-irradiation significantly attenuated the radiation-induced oxidative stress in heart tissues which was substantiated by a significant amelioration of serum LDH, CPK and AST activities. GSE treatment also attenuated the oxidative stress in pancreas tissues which was associated with a significant improvement in radiation-induced hyperglycemia and hyperinsulinemia. In conclusion, the present data demonstrate that GSE would protect the heart and pancreas tissues from oxidative damage induced by ionizing irradiation.Phytotherapy Research 03/2009; 23(3):434-8. DOI:10.1002/ptr.2684 · 2.40 Impact Factor