Puerarin from Pueraria lobate attenuates ischemia‐induced cardiac injuries and inflammation in vitro and in vivo: The key role of miR‐130a‐5p/HMGB2 pathway

Abstract

AbstractAcute 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.