摘要
目的:研究新型化合物甲胺鸢尾素(methyl-amine irisolidone,MMI)预处理对H2O2损伤大鼠心肌细胞线粒体膜电位变化的影响。方法:甲胺鸢尾素预处理心肌细胞12 h后,采用H2O2诱导细胞氧化应激损伤,瑞氏-吉姆萨染色观察细胞形态,MTT法检测细胞存活率,流式细胞仪检测细胞线粒体膜电位变化。结果:与正常对照组比较,模型组心肌细胞存活率明显降低(P<0.01)。MMI0.1μmol/L组与模型组相比细胞存活率相近(P>0.05),0.5、1、5、10μmol/L组显著增高(P<0.05,P<0.01)。与模型组比较,10μmol/L MMI减轻细胞形态变化,1、5、10μmol/L MMI显著抑制线粒体膜电位下降(P<0.05,P<0.01)。结论:甲胺鸢尾素可改善H2O2所致心肌细胞氧化应激损伤,其机制与稳定细胞膜、抑制线粒体膜电位下降,进而抑制心肌细胞凋亡有关。
AIM： To investigate the protective effect of methylamine irisolidone （MMI） preconditioning on mitochondrial membrane potential in H2O2 -induced rat cardiomyocytes injury. METHODS： With the pretreatment of methylamine irisolidone for 12 h in the model of H2O2 -induced injury, the cell viability was determined by MTT assay, and the morphology change was examined with Wright＇ s staining and Giemsa＇ s staining, and the change of mitochondrial membrane potential was analyzed by flow cytometry. RESULTS： Compared with the normal group, the cell viability of model group was significantly decreased （ P 〈 0.01 ）. Pretreated with methylamine irisolidone （0.5, 1, 5, 10 μmol/L） the cell viabilities were increased significantly （P 〈0.05, P 〈 0.01）, but MMI 0.1μmol/L group had the similar cell viability compared with the model group （ P 〉 0.05）. Moreover, pretreated with methylamine irisolidone （1, 5, 10μmol/L） the mitochondrial membrane potential were increased （P 〈 0.05, P 〈 0.01 ）, and 10 μmol/L group reduced the cell morphology injury. CONCLUSION： Methylamine irisolidone can improve the morphology injury of cadiocytes induced by H2O2 and increase the mitochondrial membrane potential, which can decrease the cadiocyte apoptosis.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2009年第6期613-616,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
国家自然科学基金资助项目(30701022)
山东省自然科学基金项目(Y2007C156)
关键词
甲胺鸢尾素
心肌细胞
线粒体膜电位
氧化应激
细胞凋亡
methylamine irisolidone
cadiocyte
mitochondnal membrane potential
oxidative stress
apoptosis
