The incidence of type II diabetes caused by islet cell injury is increasing in recent years. Endoplasmic reticulum stress is one of the crucial causes of islet β 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 β 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 α, ATF-4 and CHOP) by western
blotting. Next the lentivirus was used to construct the islet 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 β cells
were detected by flow cytometry. We found that high glucose medium promoted the expression of p-PERK, p-Eif2 α, ATF-4 and CHOP while downregulated the levels of SERP1 in isletβ cells. Moreover, overexpression of SERP1 induced the downregulation of levels of p-PERK, p-Eif2 α,
ATF-4, CHOP, TNF-α , IL-1β and IL-6 and alleviated the apoptosis of islet cells. At last, the overexpression of CHOP rescued the apoptosis rates and the expression of TNF-α, IL-1β and IL-6. These results indicated SERP1 relieved the inflammation response and apoptosis
of islet β cells by inhibiting the expression of CHOP and alleviating the endoplasmic reticulum stress induced damage.
Myricetin Protects Against High Glucose-Induced β-Cell Apoptosis by Attenuating Endoplasmic Reticulum Stress via Inactivation of Cyclin-Dependent Kinase 5