Mechanism of Increased Myocardial Ischemic Vulnerability in Mice Type 2 Diabetes Mellitus Induced by Endoplasmic Reticulum Stress / 中国循环杂志

ABSTRACT

Objective: To study the relationship between endoplasmic reticulum stress (ERS) and adiponectin;to explore the role of ERS for increasing myocardial ischemic vulnerability in type 2 diabetes mellitus (DM) mice. Methods: Type 2 DM model was established by high fat diet with streptozotocin (STZ) injection. A total of 35 C57BL/6J male type 2 DM mice were divided into 4 groups: ①Control group, n=5. ②Tauroursodeoxycholic acid (TUDCA) group,③Thapsigargin (TG) group and ④Normal saline group. The mice in Groups ②, ③, ④were fed by high fat and high glucose diet by injecting streptozotocin (STZ), in the last 3 weeks and respectively received intraperitoneal injections of TUDCA (250 mg/kg), thapsigargin (TG) (300μg/kg) and normal saline twice a day, n=10 in each group. Then myocardial infarction (MI) model was established in 5 mice from each group. 72 hours later, the MI ranges were measured, serum levels of adiponectin were detected, mRNA expressions of adiponectin and CHOP in myocardial tissue were examined. Results: The MI range in TUDCA group (21.47 ± 2.85)%and in Normal saline group (39.92 ± 4.28)%were both lower than TG group (66.56 ± 8.15)%, both P Conclusion: ESR could increase myocardial vulnerability in type 2 DM mice which might be related to down-regulating adiponectin expression.