IL-1β And High Concerntration Glucose Synergically Induce SD Rat Islet Dealth Via Stimulation Of ERK Activation

Diabetes threat humane being's health all over the world, elucidating the mechanism plays a crucial role in the cure and prevention of diabetes. The mass of beta cell is requisite for insulin secretion, and the dysfunction makes it eventually develop to diabetes. Current opinion that the onset of diabetes is closely related to cell inflammation has been widely accepted. As a mediator of inflammation, the relationship between diabetes and IL-1 has been emphasized for a long time. IL-1 can initiate the influx of Ca2+, and stimulate the ERK signal transduction, which is a component of MAPK famlily, and therefore exert important roles in beta cell death. On the other, glucose is the main mediator of beta cell function, and control insulin synthesis and release. Chronic high concentration glucose causes beta cell dysfunction.We use the islets separated from SD rat as experimental material, investigate how to induce beta cell death via stimulating ERK activity.