论文部分内容阅读
目的观察活性氧物质(Reactive oxygen species,ROS)在多柔比星(Doxorubicin,Dox)诱导的心肌细胞凋亡中的作用。方法将大鼠胚胎期心肌细胞H9C2分为对照组、Dox 0.1μmol/L组和Dox 1.0μmol/L组,Dox作用24 h后,采用硫代巴比妥酸(Thibatituric acid,TBA)法检测丙二醛(Malondialchehyche,MDA)含量;血浆三价铁降低能力法(Ferric reducing ability of plasma,FRAP)检测总抗氧化能力(Total antioxidation capability,T-AOC);DCFH-DA荧光探针染色法检测ROS含量;JC-1染色法检测线粒体膜电位(Mitochondrial membrane potential,△ψm);TUNEL法检测心肌细胞凋亡指数(AI)。结果与对照组相比,DOX 1.0μmol/L组MDA、ROS含量及AI显著上升(P<0.05),T-AOC及△ψm显著下降(P<0.05)。结论 Dox诱导心肌细胞凋亡过程中,ROS生成增加,超过了抗氧化体系的清除能力,氧化应激损伤机制发挥了重要作用。
Objective To observe the role of reactive oxygen species (ROS) in cardiomyocyte apoptosis induced by Doxorubicin (Dox). Methods The H9C2 cells were divided into control group, Dox 0.1 μmol / L group and Dox 1.0 μmol / L group. After 24 h treatment with Dox, Thiobarbituric acid (TBA) (MDA), plasma total antioxidant capacity (T-AOC) in the plasma ferric reducing ability of plasma (FRAP), ROS detection by fluorescent dye DCFH-DA Content; Mitochondrial membrane potential (△ ψm) was detected by JC-1 staining; apoptosis index (AI) was detected by TUNEL method. Results Compared with the control group, the content of MDA and ROS and the content of AI in DOX 1.0μmol / L group increased significantly (P <0.05), while T-AOC and △ ψm decreased significantly (P <0.05). Conclusion Dox induces cardiomyocyte apoptosis in a dose-dependent manner and increases ROS production, which exceeds the scavenging capacity of antioxidant system and plays an important role in oxidative stress injury.