Document Type: Research Paper
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
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.