Aloperine Regulates Inflammation, Apoptosis, and Autophagy in H9C2 Rat Cardiomyoblast Cells After Excessive Hypoxia

Abstract

Myocardial infarction (MI) is a cardiovascular condition that leads to increased morbidity and mortality, impacting the quality of life of individuals. Aloperine (ALO), derived from Sophora alopecuroides L, has been recognized for its beneficial effects in treating various diseases by showcasing therapeutic properties. However, the precise protective mechanisms of ALO on hypoxia/reoxygenation (H/R) -induced damage in cardiomyocytes in vitro remain unclear. In this study, it was manifested that cell proliferation was weakened after H/R treatment, but this impact was offset after ALO treatment. Furthermore, cell apoptosis was heightened after H/R treatment, but this phenomenon was neutralized after ALO treatment. ALO relieved inflammation in H/R-treated H9C2 rat cardiomyoblast cells. Moreover, ALO strengthened autophagy in H/R-triggered H9C2 rat cardiomyoblast cells through enhancing the LC3II/LC3I level and the LC3B fluorescence intensity. Lastly, it was testified that ALO can rescue the weakened autophagy, the heightened cell apoptosis, and the augmented inflammation after CC treatment in H/R-mediated H9C2 rat cardiomyoblast cells. In conclusion, ALO regulated inflammation, apoptosis, and autophagy through AMPK/Nrf2 pathway in H9C2 rat cardiomyoblast cells after excessive hypoxia. This study suggested that ALO may be an underlying drug for MI therapy.