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.