Effect of autophagy on myocardial infarction and its mechanism

To investigate the effect of autophagy on acute myocardial infarction (AMI), and its mechanism in rats.

A total of 75 Sprague Dawley (SD) rats were randomly divided into three groups (n=25): sham operation (S) group, the AMI group and rapamycin (RAPA) treatment group. The model of AMI was established and the myocardial infarction size was calculated by triphenyltetrazolium chloride (TTC) staining. Morphological changes in myocardium were observed by hematoxylin and eosin (HE) staining. Expression levels of autophagy-related proteins LC3-phosphatidylethanolamine conjugate (LC3-II) and p62 were detected by semi-quantitative polymerase chain reaction (PCR) and Western blot.

Compared with the S group, the heart-to-body weight ratio on the 21st day in AMI group was significantly increased. TTC staining results showed that compared with the S group, the size of left ventricular infarction area was significantly increased in the AMI group, and that in the RAPA group was significantly decreased. HE staining results showed that the anterior wall of the left ventricle of rats became thinner, and myocardial cells were degenerated and lost seriously in the AMI group 21 days later. Compared with the S group, the expression level of LC3-II in the infarcted peripheral area was significantly increased and that of p62 was significantly increased in the AMI group. Compared with the AMI group, the expression level of LC3-II in the infarction-peripheral area was significantly increased and that of p62 was significantly decreased after the treatment with RAPA.

Autologous activation could protect myocardium by the left anterior descending (LAD) ligation in rats. Autophagy could reduce the area of myocardial infarction after LAD ligation and improve cardiac function.