目的研究阿魏酸(FA)对阿霉素(DOX)诱导H9c2心肌细胞损伤的影响。方法 1μmol·L-1DOX处理H9c2细胞24 h,建立心肌损伤模型。FA预处理组,10、20、40μmol·L-1FA预处理2 h后,再与DOX共培养24 h。CCK-8比色法测定细胞生存率;相差显微镜观察细胞形态学改变;生化试剂盒检测LDH、CK、MDA、SOD;DCF-DA荧光染色流式细胞术检测细胞内活性氧;AO-EB染色、DNA琼脂糖凝胶电泳检测细胞凋亡;Western blot法测定caspase-3、Bax、Bcl-2表达。结果 DOX降低H9c2细胞生存率,诱导氧化应激损伤和细胞凋亡。FA预处理剂量依赖性提高细胞生存率,减轻LDH、CK外漏和损伤细胞形态学改变。FA减少ROS生成,降低细胞MDA水平,增加SOD酶活性,抑制DOX诱导的氧化应激。FA下调促凋亡蛋白caspase-3和Bax,上调凋亡抑制蛋白Bcl-2,减少心肌细胞凋亡。结论 FA可抑制DOX诱导的氧化应激和心肌细胞凋亡,减轻心肌损伤。 Objective To investigate the effect of ferulic acid (FA) on doxorubicin (DOX) -induced injury of H9c2 cardiomyocytes. Methods H9c2 cells were treated with 1μmol·L-1DOX for 24 hours to establish a myocardial injury model. FA pretreatment group, 10,20,40μmol·L-1FA pretreatment 2 h, then co-cultured with DOX 24 h. Cell viability was measured by CCK-8 colorimetric assay. Cell morphological changes were observed by phase contrast microscopy. LDH, CK, MDA and SOD were detected by biochemical kit. Reactive oxygen species (ROS) were detected by flow cytometry with DCF-DA staining. The apoptosis was detected by DNA agarose gel electrophoresis. The expressions of caspase-3, Bax and Bcl-2 were detected by Western blot. Results DOX decreased the survival rate of H9c2 cells and induced oxidative stress injury and apoptosis. FA pretreatment dose-dependently increased cell survival rate, reduced LDH, CK leakage and injury cell morphology changes. FA reduces ROS production, decreases cellular MDA levels, increases SOD activity, and inhibits DOX-induced oxidative stress. FA down-regulates pro-apoptotic proteins caspase-3 and Bax, up-regulates apoptosis-inhibiting protein Bcl-2 and decreases cardiomyocyte apoptosis. Conclusion FA can inhibit DOX-induced oxidative stress and myocardial apoptosis, reduce myocardial injury.