Puerarin protects pancreatic β-cell survival via PI3K/Akt signaling pathway

Pancreatic beta-cell loss because of apoptosis is the major cause of type 1 diabetes (T1D) and late stage T2D. Puerarin possesses anti-diabetic properties; whether it acts directly on pancreatic beta-cell is not clear. This study was designed to investigate the effects of puerarin on pancreatic beta-cell survival and function. Diabetes was induced in male C57BL/6 mice by a single peritoneal injection of streptozotocin (STZ). Pancreatic beta-cell survival and function were assessed in diabetic mice by measuring beta-cell apoptosis, beta-cell mass, pancreatic insulin content, and glucose tolerance, and in cultured islets and clonial MIN6 beta-cells by measuring beta-cell viability and apoptosis and glucose-stimulated insulin secretion. We found that pre-treatment with puerarin decreased the incidence of STZ-induced diabetes. Puerarin increased pancreatic beta-cell mass via beta-cell apoptosis inhibition in diabetic mice, and increased serum insulin, whereas it decreased blood glucose levels and improved glucose tolerance. In cultured islets and MIN6 cells, puerarin protected beta-cell from cobalt chloride (CoCl2)-induced apoptosis and restored the impaired capacity of glucose-stimulated insulin secretion. Puerarin protection of beta-cell survival involved the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. In conclusion, puerarin protects pancreatic beta-cell function and survival via direct effects on b-cells, and its protection of beta-cell survival is mediated by the PI3K/Akt pathway. As a safe natural plant extraction, puerarin might serve as a preventive and/or therapeutic approach for diabetes.