Asperulosidic Acid Attenuates Myocardial Ischemia-Reperfusion Injury and Suppresses MAPK Signaling

This study evaluated the protective effects of asperulosidic acid (ASP) against myocardial ischemia/reperfusion (I/R) injury and investigated the underlying mechanisms. An in vitro oxygen-glucose deprivation/reoxygenation model was established in H9c2 cells, and an in vivo rat I/R model was generated by left anterior descending coronary artery ligation. ASP treatment significantly improved cell viability and reduced apoptosis in vitro. In vivo, ASP decreased myocardial infarct size, alleviated histopathological damage, and reduced serum creatine kinase and lactate dehydrogenase levels. Additionally, ASP suppressed inflammatory cytokine expression, reduced reactive oxygen species and malondialdehyde levels, enhanced antioxidant enzyme activities, and inhibited myocardial apoptosis. Network pharmacology and molecular docking identified the MAPK signaling pathway as a potential target. Mechanistically, ASP reduced the phosphorylation of p38, ERK, and JNK in myocardial tissue. These findings demonstrate that ASP attenuates myocardial I/R injury by reducing oxidative stress, inflammation, and apoptosis, associated with suppression of the MAPK signaling pathway.