The protective effect of Nrf2/ARE pathway on islet B cell in type 2 diabetic rats / 中华内分泌外科杂志

ABSTRACT

Objective To investigate the effects of Nrf2/ARE pathway activator upregulating the expression of phase Ⅱ detoxifcation enzymes and antioxidant enzymes in islet B cell on its morphological structure in type 2 diabetic rats.Methods Type 2 diabetic rats were divided into diabetes model group (DM group),and tertiary-Butylhydroquinone intervention group(tBHQ group).At the same time,the normal control group (NC group)was set up.All rats were killed after eight-week continuous intervention.Fasting blood glucose (FBG) and fasting insulin (FINS) level were determined.Morphological structure of islet cells and apoptosis were observed.ELISA was used to determine MDA,TNF-α and T-SOD levels in serum and pancreatic tissues and Western blot was used to detect the protein expression levels of total Nrf2 and nulear Nrf2 in pancreatic tissues.Results Compared with NC group,FBG and FINS levels significantly increased and decreased in DM group respectively (all P=0.000).Compared with DM group,FBG and FINS levels significantly decreased and increased in tBHQ group respectively (all P=0.000).Compared with NC group,the number of islet cells significantly decreased and swelling,necrosis and apoptosis occurred in DM group.Islet cells in tBHQ group were significantly better than those in DM group.Compared with NC group,MDA and TNF-α levels in serum and pancreatic tissue significantly increased and TSOD levels significantly decreased in DM group (all P=0.000).Compared with DM group,MDA and TNF-α levels in serum and pancreatic tissue significantly decreased and T-SOD levels significantly increased in DM group(all P=0.000).Total Nrf2 and nulear Nrf2 in protein expression in DM group were significantly lower of than those in NC group (P()=0.000,P nulear Nrf2=0.006).Rats in tBHQ group had significantly higher protein expression of total Nrf2 and nulear Nrf2 than in DM group (all P=0.000).Conclusions Activating Nrf2/ARE pathway can reduce injury of oxidative stress and chronic inflammation on islet B cells further through upregulating the expression of phase Ⅱ detoxifying enzymes and antioxidant enzymes in islet B cells.