CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose.

CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose. Exp Ther Med. 2018 May;15(5):4213-4222 Authors: Yang W, Wu F, Luo T, Zhang Y Abstract Diabetic patients are more sensitive to ischemic injury than non-diabetics. Endoplasmic reticulum (ER) stress has been reported to be closely associated with the pathophysiology of ischemic injury in diabetes. The aim of the present study was to investigate the mechanisms involved in the progression of diabetes complicated by myocardial infarction (MI) and further verify the role of CCAAT/enhancer binding protein (C/EBP)-homologous protein (CHOP) using an in vitro model of diabetes/MI. The rats were exposed to 65 mg/kg streptozotocin (STZ) and left anterior descending (LAD) coronary artery ligation. ST-segment elevation, heart rate, left ventricular systolic pressure (LVSP) and LV end-diastolic pressure (LVEDP) were measured. Serum creatinine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were examined by ELISA. Infarct size and apoptosis were measured by triphenyltetrazolium chloride staining and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay. Pathological changes were evaluated by hematoxylin and eosin staining. H9c2 cells were used to establish an in vitro model of diabetes complicated by MI. Following CHOP knockdown, cell viability, cell cycle distribution and...
Source: Experimental and Therapeutic Medicine - Category: General Medicine Tags: Exp Ther Med Source Type: research