Conclusion
Myocardial ischemia-reperfusion can enhance autophagy response and promote apoptosis. CA plays a protective role in myocardium by targeting ATG12, thereby inhibiting autophagy and improving myocardial cell apoptosis.
Methods
The MI/RI model was established by the ligation of the left anterior descending coronary artery with ischemia and reperfusion. In vitro cell models were established using hypoxia/reoxygenation. Western blot was used to determine the expression levels of beclin-1, P62, and LC3 II. The expression levels of IL-1β, IL-6, TNFα, and apoptosis-related genes Bax, Cyt-c, and Bcl-2 were detected by qRT-PCR. Cell activity was detected by CCK-8. Apoptosis was detected by TUNEL staining.
Objective
To investigate the effect of CA on autophagy and its molecular mechanism after myocardial ischemia/reperfusion injury (MI/RI).
Results
Beclin-1, P62, and LC3 II protein expression and LC3 II/LC3 I level were significantly increased after myocardial ischemia-reperfusion injury. Compared with model group, CA downregulated beclin-1, P62, and LC3 II protein expression and LC3 II/LC3 I level in the myocardium. The results of cell-level experiments showed that CA inhibited the autophagy response of the cardiomyocytes induced by hypoxia-reperfusion injury. Mechanism studies showed that CA targeted the inhibition of ATG12. Knocking down ATG12 reduces the production of inflammatory cytokines induced by H/R. The knockdown of ATG12 also reduced apoptosis and injury of the myocardial cells.