salvianolic acid b improves insulin secretion from interleukin 1β-treated rat pancreatic islets: the role of pi3k-akt signaling

Background and objective: oxidative stress induced by proinflammatory cytokines such as il-1β plays a major role in β-cell destruction in diabetes type 1. salvianolic acid b (sal b) is a polyphenolic compound with antioxidant and protective effects. thus, objective of this study was to assess the protection exerted by sal b on isolated rat islets exposed to il-1β and to investigate an underlying mechanism in vitro. materials and methods: isolation of pancreatic islets was done by using the collagenase digestion method. isolated rat islets were divided into 6 groups including: 1. control, 2. interleukin-1β treated, 3 and 4. interleukin-1β treated+ sal b, 5 and 6. interleukin-1β treated+ sal b+ pkb and pi3k inhibitors. interleukin-1β (1 u/ml) was used to induce cytotoxicity after pretreatment with two doses of sal b (50 μm and 100 μm) and application of each inhibitors was before sal b. results: il-1β significantly decreased insulin secretion from isolated islets. pretreatment with sal b ameliorated the effect of il-1β on glucose stimulated insulin secretion in a concentration dependent manner. inhibitors of pkb and pi3k both abolished these improving effect of sal b. conclusion: sal b that has antioxidant, anti inflammatory and anti apoptotic properties, provided resistance to pancreatic β-cell dysfunction from cytokine in part via pi3k/akt pathway. the findings represent that it is a promising agent for prevention of β-cell dysfunction in type 1 diabetes.