Polyphyllin I improves myocardial damage in coronary artery disease via modulating lipid metabolism and myocardial apoptosis.

Polyphyllin I (PPI) is a famous traditional medicine ingredient, which has been explored in wide range of areas. Nevertheless, whether PPI exerts any functions in coronary artery disease (CAD) is still uncertified. Herein, we probed the effect and mechanism of PPI on lipid metabolism and myocardial dysfunction in myocardial cells and CAD rat model. Hypoxia/reoxygenation (H/R)-treated H9c2 cells model was constructed for the in vitro experiments, and CAD model in vivo was established by high-fat feeding. After management with PPI, the correlated factors of lipid metabolism and myocardial function were investigated. The apoptosis of myocardial cells was assessed by Annexin V-FITC/PI kit and TUNEL staining. The apoptosis-associated factors (caspase 3, cleaved caspase 3, Bax, and Bcl-2) were tested by Western blot analysis. The MEK/ERK inhibitor was applied and the functions of MEK/ERK pathway in myocardial damage were investigated. H/R-treated H9c2 cells model was constructed for the in vitro experiments, and CAD model in vivo was established by high-fat feeding. After management with PPI, the correlated factors of lipid metabolism and myocardial function were investigated. The apoptosis of myocardial cells was assessed by Annexin V-FITC/PI kit and TUNEL staining. The apoptosis-associated factors (caspase 3, cleaved caspase 3, Bax, and Bcl-2) were tested by Western blot analysis. The MEK/ERK inhibitor was applied and the functions of MEK/ERK pathway in myocardial damage were investigated. PPI improved lipid metabolism disorder in H/R-induced H9c2 cells or in CAD rat model. Additionally, PPI attenuated myocardial dysfunction in CAD rats via enhancing left ventricular systolic pressure, maximum rate of change of left ventricular pressure (±dp/dtmax ), and arterial blood flow (CF). The apoptosis of myocardial cells was lessened by PPI management, which was further verified by reducing Bax and cleaved caspase 3 expression. Furthermore, PD0325901 (MEK/ERK inhibitor) weakened the effect of PPI on myocardial dysfunction, lipid metabolism, and myocardial cell apoptosis in CAD rats. The research confirmed the protective effect of PPI on myocardial damage in CAD, which was regulated by MEK/ERK pathway.