Protective effect of glycyrrhizin on coronary microembolization-induced myocardial dysfunction in rats.
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ABSTRACT: 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-?, iNOS, IL-6, IL-1?, 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-?B signaling pathway was analyzed. Glycyrrhizin prevented CME-induced production of HMGB1, TNF-?, iNOS, IL-6, and IL-1?. 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-?B signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.
SUBMITTER: Yuan Y
PROVIDER: S-EPMC7842630 | biostudies-literature | 2021 Feb
REPOSITORIES: biostudies-literature
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