Dipeptidyl peptidase-4 inhibitor impacts the expression of Bcl-2 and Bax throughγamino acid bwtyric acid in pancreas islets / 中华内分泌代谢杂志

ABSTRACT

Objective To explore the effects of dipeptidyl peptidase ( DPP-4 ) inhibitor on proteins expression of Bcl-2 and Bax of islet β-cells through increasing the expression of islet γ amino acid butyric acid ( GABA) . Methods A total of 50 rats of clean grade were studied. Among them, ten rats were randomly selected as normal controls, the remaining forty rats were fed with high-fat diet and then intraperitoneal injection with streptozotocin, the diabetic rats models were then established. Rats were randomly divided into three groupsi. e. diabetic control group, DPP-4 inhibitor group, and antagonist group ( DPP-4 inhibitor and GABA receptor antagonist). Six weeks later, blood glucose, serum insulin, glucagon, and the proteins expression of GABA, Bcl-2, and Bax of islet β-cells were measured. Results ( 1 ) Compared with diabetic control group, serum insulin was increased(P<0.05),bloodglucoseandserumglucagonweredecreasedinDPP-4inhibitorgroup(P<0.05). (2) Compared with DPP-4 inhibitor group, serum insulin was decreased(P<0. 05), blood glucose and serum glucagon were increased(P<0. 05) in antagonist group. (3) Compared with diabetic control group, the expression of GABA was increased(P<0. 05), the expression of Bcl-2 protein was increased (P<0. 05) in pancreatic β-cells in DPP-4 inhibitor group. ( 4 ) Compared with diabetic control group, the expression of GABA in pancreatic β-cells was increased in antagonist group(P<0. 05) . Compared with DPP-4 inhibitor group, the expression of Bax protein in pancreaticβ-cells was increased in antagonist group(P<0. 05) , while the expression of Bcl-2 protein was decreased (P<0. 05). Conclusions DPP-4 inhibitor could increase the secretion of insulin, decrease the secretion of glucagon, up-regulate expression of anti-apoptosis protein Bcl-2, and down-regulate expression of apoptosis protein Bax in pancreatic β-cells through increasing the expression of GABA, inhibiting pancreatic β-cells apoptosis and protecting the damagedβ-cells in type 2 diabetic rats.