Abstract
Acute myocardial infarction (AMI) is a common cardiovascular disease and puerarin (Pue) is an active compound from Pueraria lobate with cardio-protective potential. In the current study, the mechanism underlying the cardio-protective effects of Pue was explored by focusing miR-130a-5p/HMGB2 pathway. MiR expression profile was determined and myocardial infarction was induced in cardiomyocytes and rats, which was treated with Pue. The role of miR-130a-5p and downstream HMGB2/NF-κB axis in the cardio-protective effects of Pue was also explored. Pue increased viability and suppressed inflammation in OGD cardiomyocytes, which was associated with the deactivation of HMGB2/NF-κB pathway. After the suppression of miR-130a-5p, the cardio-protective effects of Pue were compromised. In rat models, Pue attenuated structure deterioration and inflammatory response in heart. At the molecular level, miR-130a-5p was up-regulated, and HMGB2 were down-regulated. It was demonstrated that Pue induced the expression of miR-130a-5p, which suppressed the activity of HMGB2/NF-κB, contributing to the attenuation of infarct heart tissues.