Platycodin D protects pancreatic β-cells from STZ-induced oxidative stress and apoptosis

Abstract Diabetes mellitus is a group of physiological dysfunctions associated with hyperglycemia-mediated oxidative stress and apoptosis in pancreatic β-cells. Platycodin D (PLD) is a major saponin isolated from Platycodon grandiflorum that has been reported to possess many pharmacological effects including anti-oxidative, anti-apoptotic and anti-diabetic. In the present study, we evaluated the effects of PLD on oxidative stress and apoptosis in INS-1 cells exposed to streptozotocin (STZ). Our results showed that PLD improved STZ-caused reduction in cell viability of INS-1 cells. PLD prevented STZ-induced apoptosis in INS-1 cells with decreased bax expression and caspse-3 activity, as well as increased bax expression. PLD decreased ROS production and increased SOD activity in STZ-induced INS-1 cells. Treatment with PLD also improved the insulin secretion capacity and the expression of insulin1/2 in STZ-induced INS-1 cells. Furthermore, PLD suppressed the STZ-induced activation of p38 pathway, while enhanced the activation of Nrf2/HO-1 pathway in INS-1 cells. Treatment with p38 agonist (p79350) or knockdown of Nrf2 reversed the protective effects of PLD on INS-1 cells. Taken together, PLD protects INS-1 cells from STZ-induced oxidative stress and apoptosis. The protective effect of PLD might be ascribed to the regulation of p38 and Nrf2 pathways.