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Title: The reduction of hypoxia-induced and reoxygenation-induced apoptosis in rat islets by epigallocatechin gallate. Author: Hara Y, Fujino M, Adachi K, Li XK. Journal: Transplant Proc; 2006 Oct; 38(8):2722-5. PubMed ID: 17098050. Abstract: The survival of transplanted tissue is affected by the detrimental consequences of hypoxia followed by reoxygenation. The majority of transplanted cells undergo apoptosis due to hypoxia and reoxygenation (H/R) injury, but protection from H/R has been less examined. In this study, we examined whether epigallocatechin gallate (EGCG) protected rat islets from H/R injury. Rat islets, freshly prepared from F344 rat strain by collagenase digestion and density centrifugation, were seeded in triplicate at concentrations of 100 per well in 24-well plates for culture under normoxia. The cells were then exposed to hypoxia for 14 hours with or without EGCG, after which they were reoxygenated for 72 hours in a humidified oxygenated CO(2) incubator at 37 degrees C. Apoptosis, lactate dehydrogenase (LDH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were evaluated according to the manufacturer's instructions. The H/R induced apoptosis in the islets that was reduced in dose-dependent manner by EGCG treatment. The viability of islets exposed to H/R was assessed by LDH release. H/R reduced viability compared with the controls, while the viability of the islets improved upon EGCG treatment. The secretion of insulin was also decreased by H/R, as well as the dose dependent EGCG protective ability on insulin secretion. The content of 8-OHdG in islets from H/R was also reduced by EGCG. Our results indicated that apoptosis and the decline in insulin secretion by H/R were inhibited by EGCG treatment. EGCG may be considered useful for protection of islets from oxidative injury associated with the transplantation procedure.[Abstract] [Full Text] [Related] [New Search]