Diallyl trisulfide modulated autophagy in isoproterenol induced acute myocardial infarction

Background Acute myocardial infarction (AMI) is the most serious manifestation of coronary artery disease. The initial ischemia in AMI causes biochemical and metabolic alterations in cardiomyocytes. Objectives The present study aimed to investigate the biomolecular mechanisms underlying cardioprotective effects of diallyl trisulfide (DATS) as well as captopril (CAP) in isoproterenol (ISO) induced AMI focusing on autophagy & PI3K/Akt signaling. Methods Seventy male Albino rats were divided into seven groups as follows: Normal control, ISO, ISO + LY294002 (PI3K inhibitor), DATS+ISO, CAP+ISO, DATS+LY294002 + ISO, and CAP+LY294002 + ISO. All treatments (40 mg/kg DATS, 50 mg/kg CAP & 0.3 mg/kg LY294002) were given daily for two weeks before ISO injection (85 mg/kg for 2 days). At the end of the experiment, serum and cardiac tissues were collected. Serum cardiac troponin I (cTnI), and creatine kinase MB (CK-MB) were measured. Cardiac glutathione peroxidase (GSH-px), malondialdehyde (MDA), hypoxia-inducible factor 1 alpha (HIF-1α), autophagy proteins (P62 & LC3IIB) and gene expression of PI3K, Akt, FOXO-1, and eNOS were assessed. Histopathological examination of heart tissue was performed. Results DATS and CAP significantly ( p