苦参碱对阿霉素所致H9c2心肌细胞损伤的保护作用及与线粒体Na+-K+-ATP酶、Ca2+-ATP酶关系的研究

目的：研究苦参碱对阿霉素所致H9c2心肌细胞损伤的保护作用及其机制。方法：将H9c2心肌细胞培养，取2~3代细胞进行试验，共分为4组。对照组：接受生理盐水作为干预因素；阿霉素组：接受0.5 mg·L^-1阿霉素作为损伤模型；苦参碱+阿霉素组：接受0.5 mg·L^-1阿霉素和不同浓度苦参碱（50，150，200 mg·L^-1）作为干预因素；苦参碱组：接受不同浓度苦参碱（50，150，200 mg·L^-1）作为干预因素。以上各组相应干预24 h后，应用流式细胞仪检测H9c2心肌细胞凋亡水平，应用分光光度法检测线粒体Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶活性，利用JC-1法检测线粒体膜电位。结果：与阿霉素组相比，苦参碱+阿霉素组H9c2心肌细胞凋亡显著减少、线粒体Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶活性显著升高（P<0.05）、线粒体膜电位显著改善。结论：苦参碱对阿霉素所致H9c2心肌细胞有保护作用，减轻心肌细胞凋亡，改善线粒体膜电位、提高线粒体Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶活性。

Protective effect of matrine on H9c2 cardiomyocyte injury induced by adriamycin and its relationship with mitochondrial Na+-K+-ATPase and Ca2+-ATPase

OBJECTIVE To study the protective effect and mechanism of matrine on H9c2 cardiomyocytes injury induced by adriamycin.METHODS H9c2 cardiomyocytes were cultured and 2-3 passages of cells were used for testing.They were divided into 4 groups.Control group:received normal saline as intervention factor;adriamycin group:received 0.5 mg·L^-1 adriamycin as injury model;matrine+adriamycin group:received 0.5 mg·L^-1 adriamycin and different concentrations of matrine (50,150,200 mg·L^-1) as an intervention factor; matrine group:received different concentrations of matrine (50,150,200 mg·L^-1) as an intervention factor.After 24 hours of intervention,the apoptosis of H9c2 cardiomyocytes was detected by flow cytometry.The mitochondrial Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities were detected by spectrophotometry.The mitochondrial membrane potential was detected by JC-1 method. RESULTS Compared with the adriamycin group,the apoptosis of H9c2 cardiomyocytes in the matrine+adriamycin group was significantly decreased,and the mitochondrial Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities were significantly increased (P<0.05).Mitochondrial membrane potential is significantly improved.CONCLUSION Matrine has protective effect on H9c2 cardiomyocytes induced by adriamycin,reduces cardiomyocyte apoptosis, improves mitochondrial membrane potential,and increases mitochondrial Na⁺-K⁺-ATPase and Ca²⁺-ATPase activities.