Protective effect of glycyrrhizin on coronary microembolization‐induced myocardial dysfunction in rats

Coronary microembolization (CME)‐induced inflammation and cardiomyocyte apoptosis are two key factors contributing to CME‐induced myocardial dysfunction. High‐mobility group box‐1 (HMGB1) plays essential role in progression of CME‐induced injury and inhibition of HMGB1 has been shown to be protective. In present study, the potential effects of glycyrrhizin, a HMGB1 inhibitor, on CME‐induced myocardial dysfunction are evaluated. Using a rat model of CME, we administrated glycyrrhizin in rats prior to CME induction. The level of HMGB1, TNF‐α, iNOS, IL‐6, IL‐1β, cleaved caspase‐3, Bax, and Bcl‐2 were measured. The serum level of cardiac troponin I, creatine kinase, was detected. The cardiac function and cardiomyocyte apoptosis were evaluated. The activation of TLR4/NF‐κB signaling pathway was analyzed. Glycyrrhizin prevented CME‐induced production of HMGB1, TNF‐α, iNOS, IL‐6, and IL‐1β. Glycyrrhizin inhibited CME‐induced cardiomyocyte apoptosis and the expression of cleaved caspase‐3 and Bax, while enhanced the expression of Bcl‐2. Glycyrrhizin decreased cardiac troponin I and creatine kinase levels and improved cardiac function. Glycyrrhizin prevented the activation of HMGB1/TLR4/NF‐κB signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.
Glycyrrhizin prevented CME‐induced production of HMGB1, TN‐α, iNOS, IL‐6, IL‐1β. Glycyrrhizin inhibted CME‐induced cardiomyocyte apoptosis and the expression of cleaved caspase‐3 and Bax, while enhanced the expression of Bcl‐2. Glycyrrhizin decreased cardiac troponin I and creatine kinase levels and improved cardiac function. Glycyrrhizin prevented the activation of HMGB1/TLR4/NF‐κB signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.