胡黄连苷Ⅱ对乙醇诱导的H9C2心肌细胞损伤的保护作用

Protective Effect of Picroside Ⅱ against Alcohol-induced Injury in H9C2 Cardiomyocytes

目的探讨胡黄连苷Ⅱ对乙醇所致H9C2心肌细胞损伤的保护作用。方法用MTT检测细胞存活率，LDH、SOD、Gpx、MDA及ROS试剂盒检测H9C2细胞在乙醇干预及胡黄连苷Ⅱ预处理条件下的氧化应激状态。结果100mmol／L及以上浓度的乙醇可导致H9C2细胞的存活率下降，100-200mmol／L之间细胞存活率下降最为明显，200mmol／L的乙醇可导致上清液中LDH活性的增加、细胞匀浆中SOD及Gpx活性的下降、细胞匀浆中MDA及细胞内ROS含量的增加。而胡黄连苷Ⅱ预处理可部分改善乙醇所致细胞存活率的下降，其保护作用部分是通过提高细胞中SOD及Gpx活性实现的。结论胡黄连苷Ⅱ对乙醇所致H9C2心肌细胞氧化应激损伤，具有保护作用，其保护作用部分是通过提高细胞的抗氧化作用实现的。

Objective To explore the cardioprotective role ofpicroside Ⅱ against alcohol-induced injury in H9C2 cardiomyocytes. Methods The cell viability and cellular damage of cardiomyocytes were respectively assessed by MTT and LDH assays. The activities of SOD and Gpx, and the contents of MDA were determined using detection kit. The levels of ROS were evaluated by inverted fluorescence microscope. Results H9C2 cell viability was decreased when treated with alcohol above 100 mmol/L, and the most significant decline was observed between 100-200 mmol./L Pretreatment of H9C2 cardiomyocytes with picmside Ⅱ （8-200 rag/L）inhibited LDH activity in culture media and increased cell viability in a dosedependent manner. This protective effect was accompanied by significantly increased activities of SOD and GSH-Px, which attenuating MDA in response to alcohol-induced injury. Fttrthermore, picmside Ⅱ also inhibited ROS production in H9C2 cardiomyocytes. Conclusion The present study demonstrated that picmside Ⅱ protects H9C2 cardiomyocytes against alcohol-induced injury through reduction of ROS production and enhancement of the activity of antioxidant defense.