Stress-Associated Endoplasmic Reticulum Protein 1 Protected High Glucose-Induced Islet beta Cells from Apoptosis by Attenuating Endoplasmic Reticulum Stress

摘要

The incidence of type II diabetes caused by islet beta cell injury is increasing in recent years. Endoplasmic reticulum stress is one of the crucial causes of islet beta cell damage, and stress-associated endoplasmic reticulum protein 1 (SERP1) could inhibit the occurrence and development of endoplasmic reticulum stress. But whether SERP1 could inhibit the damage of islet beta cell caused by endoplasmic reticulum stress is unclear. In this study, we detected the levels of SERP1 and endoplasmic reticulum stress related proteins (p-PERK, p-Eif2 alpha, ATF-4 and CHOP) by western blotting. Next the lentivirus was used to construct the islet beta cell line which was stable overexpressed SERP1. Then the expression of endoplasmic reticulum stress related proteins and inflammatory factors was determined with western blotting. At last the apoptosis rates of islet beta cells were detected by flow cytometry. We found that high glucose medium promoted the expression of p-PERK, p-Eif2 alpha, ATF-4 and CHOP while downregulated the levels of SERP1 in islet beta cells. Moreover, overexpression of SERP1 induced the downregulation of levels of p-PERK, p-Eif2 alpha, ATF-4, CHOP, TNF-alpha, IL-1 beta and IL-6 and alleviated the apoptosis of islet beta cells. At last, the overexpression of CHOP rescued the apoptosis rates and the expression of TNF-alpha, IL-1 beta and IL-6. These results indicated SERP1 relieved the inflammation response and apoptosis of islet beta cells by inhibiting the expression of CHOP and alleviating the endoplasmic reticulum stress induced damage.