Paeoniflorin protects pancreatic β cells from STZ-induced damage through inhibition of the p38 MAPK and JNK signaling pathways.

Pancreatic β-cells are responsible for insulin secretion and control of plasma glucose levels. Accumulating evidences indicate a relationship between β-cell dysfunction/death and diabetes onset. Paeoniflorin (PF), a natural glycoside, has antihyperglycemic effect. However, the role of PF in pancreatic β-cells has not been examined. The aim of this study was to evaluate the protective effect of PF on streptozotocin (STZ)-induced β-cell damage. Our results showed that PF improved STZ-caused inhibitory effect on cell viability and insulin secretion ability in INS-1 cells. PF reduced caspase-3 activity and bax expression, and induced bcl-2 expression in STZ-treated INS-1 cells. PF resulted in a decrease in production of reactive oxygen species and MDA, and an increase in SOD activity in STZ-treated INS-1 cells. Furthermore, PF inhibited the phosphorylation of p38 and JNK, which is induced by STZ in INS-1 cells. The results suggested that PF protected INS-1 cells from STZ-induced cell damage. Meanwhile, PF suppressed the activation of p38 MAPK and JNK pathways in STZ-treated INS-1 cells. These results indicated that PF might be a natural anti-diabetic agent by improving pancreatic β-cells injury through inhibition of the p38 MAPK and JNK signaling pathways.