Abstract：
We established myocardial injury models in vivo and in vitro to investigate the cardioprotective effect of gomisin D obtained from Schisandra chinensis. Gomisin D significantly inhibited isoproterenol-induced apoptosis and hypertrophy in H9C2 cells. Gomisin D decreased serum BNP, ANP, CK-MB, cTn-T levels and histopathological alterations, and inhibited myocardial hypertrophy in mice. In mechanisms research, gomisin D reversed ISO-induced accumulation of intracellular ROS and Ca2+. Gomisin D further improved mitochondrial energy metabolism disorders by regulating the TCA cycle. These results demonstrated that gomisin D had a significant effect on isoproterenol-induced myocardial injury by inhibiting oxidative stress, calcium overload and improving mitochondrial energy metabolism.
摘要：
我们在体内和体外建立了心肌损伤模型，以研究五味子的gomisinD对心脏的保护作用。GomisinD明显抑制异丙肾上腺素诱导的H9C2细胞凋亡和肥大。GomisinD降低血清BNP，ANP,CK-MB,cTn-T水平和组织病理学改变，抑制小鼠心肌肥厚。在机制研究中，gomisinD逆转ISO诱导的细胞内ROS和Ca2积累。GomisinD通过调节TCA循环进一步改善线粒体能量代谢障碍。这些结果表明，gomisinD通过抑制氧化应激对异丙肾上腺素引起的心肌损伤具有明显的作用。钙超载和改善线粒体能量代谢。
