Fas/FasL induces myocardial cell apoptosis in myocardial ischemia-reperfusion rat model.

Myocardium ischemia reperfusion is easy to induce myocardial injury. Fas/FasL is an important signaling pathway mediating cell apoptosis. This study aims to analyze the cell apoptosis and Fas/FasL expression in myocardial cell ischemia reperfusion rat model.Coronary artery ligation method was used to establish myocardial ischemia reperfusion model. Rats were grouped according to different ischemia and reperfusion time: Group A, myocardial ischemia for 30 min and reperfusion for 24 h; Group B, myocardial ischemia for 30 min and reperfusion for 48 h; Group C, myocardial ischemia for 1 h and reperfusion for 24 h. Myocardial injury indicators were tested. Myocardial cell apoptosis was detected by transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay. Fas and FasL mRNA and protein expressions were evaluated by Real-time PCR (RT-PCR) and Western blot.Creatine kinase (CK), lactic dehydrogenase (LDH), and malondialdehyde (MDA) significantly elevated, while superoxide dismutase (SOD) obviously declined in the experimental group compared with control and blank group (p<0.05). CK, LDH, and MDA gradually upregulated, whereas SOD was reduced in experimental groups following the time extension of ischemia and reperfusion (p<0.05). Apoptosis cell number was markedly higher in the experimental group compared with control and blank group (p<0.05). Apoptosis cell number gradually increased in the experimental groups following ischemia and reperfusion time extension (p<0.05). Fas/FasL mRNA and protein markedly upregulated in the experimental group compared with control and blank group (p<0.05). Fas/FasL mRNA and protein expressions enhanced in experimental groups following the time extension of ischemia and reperfusion (p<0.05).Fas/FasL induces myocardial cell apoptosis in the process of myocardium ischemia reperfusion in rat model.