Published in:
Open Access 01-12-2022 | Captopril | Original contribution
Diallyl trisulfide modulated autophagy in isoproterenol induced acute myocardial infarction
Published in: Clinical Phytoscience | Issue 1/2022
Login to get accessAbstract
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 < 0.01) decreased serum CK-MB and cTnI, cardiac levels of MDA, HIF-1α, p62 and LC3IIB along with an increase in GSH-px activity compared with ISO group. Moreover, DATS and CAP significantly up-regulated PI3K, Akt, and eNOS gene expression but down-regulated FOXO-1 expression compared to ISO group. However, LY294002 reversed DATS and CAP cardioprotective effects.
Conclusion
DATS and CAP prior treatment proved cardioprotective effects via modulation of autophagy, PI3K/Akt signaling, eNOS and FOXO-1 downregulation in ISO induced AMI rat model.