Apigenin Protects H9c2 Cells Against Oxygen-Glucose Deprivation/Reperfusion Injury by Regulating Autophagy via the HIF-1α/miR-20a Axis.

As living standards improve and the population ages, cardiovascular disease poses a significant threat to human health. Apigenin, a flavonoid compound found in many fruits and vegetables native to warm climates, is named after celery because it is found in the highest concentrations in this plant. Apigenin exhibits various physiological and pharmacological activities. However, its protective effects on the cardiovascular system and the underlying mechanisms are unclear. The aim of this study is to investigate the role of apigenin and its mechanism in protecting against myocardial cell damage induced by OGD/R in H9c2 rat myocardial cells. MTT experiments demonstrated that apigenin protects cells from OGD/R-induced damage under OGD/R conditions. Molecular mechanism studies showed that apigenin (API) inhibits HIF-1α protein expression and promotes miR-20a expression under OGD/R conditions. This reduces the expression of autophagy-related proteins, inhibits cellular autophagy, and SOD activity. Thus, API exerts a protective effect on cells under OGD/R conditions. These results suggest that apigenin protects cells from oxidative stress damage by inhibiting HIF-1α expression and promoting miR-20a expression, thereby reducing autophagy levels in H9c2 cells under OGD/R conditions.