Protective effect of wax apple (Syzygium samarangense (Blume) Merr. & L.M. Perry) against streptozotocin-induced pancreatic ß-cell damage in diabetic rats

Abstract

The purpose of this study was to investigate the protective properties and mechanisms of wax apple (Syzygium samarangense (Blume)) against streptozotocin (STZ)-induced pancreatic ß-cell apoptosis in diabetic rats. Diabetes was induced by STZ (65 mg/kg; i.p.) injection and wax apple (100 mg/kg) was orally administered to diabetic rats for a period of 30 days. During this time, fasting blood glucose (FBG) and body weight were measured weekly. At the end of the experiment, serum insulin, HOMA-B, and pancreatic insulin expression were assessed. The expression of apoptosis-related proteins along with the nitrotyrosine level, antioxidant activities, and pro-inflammatory cytokine TNF-α in the pancreas were also determined. STZ-induced diabetic rats exhibited an increase in FBG, and a decrease in body weight, serum and pancreatic insulin, as well as HOMA-B. Pancreatic apoptosis was noted in diabetic rats and indicated by enhancing the expression of cleaved caspase-3 and Bax proteins and downregulating the expression of Bcl-2 and Bcl-xl proteins. The activities of antioxidant CAT and SOD in the pancreas of the diabetic rats was also reduced. Importantly, wax apple treatment resulted in a significant reduction of FBG and increased body weight in diabetic rats. Wax apple also improved pancreatic ß-cell function, this was clearly evidenced by increased HOMA-B and pancreatic and serum insulin levels in diabetic rats. Moreover, pancreatic ß-cell apoptosis was alleviated with significantly down-regulated cleaved caspase-3 and Bax protein expression, and upregulated Bcl-2 and Bcl-xl protein expression in wax apple treated diabetic rats. These were related to the induction of CAT and SOD activities, and reduction of nitrotyrosine and TNF-α levels in wax apple administration. Overall, these results provide evidence that wax apple protects against STZ-induced pancreatic β-apoptosis and dysfunction in diabetic rats, possibly through inhibiting oxidative stress and pro-inflammatory cytokine, and activating anti-apoptotic proteins.