心肌肽素在心肌细胞氧化应激中的作用  

Effects of Cardiomyopeptidin on Hydrogen Peroxide Induced Injury in Cardiomyocytes

作　　者：朱萌[1] 张薇[1] 

机构地区：[1]山东大学齐鲁医院心内科,济南250101

出　　处：《科学技术与工程》2011年第5期932-935,共4页Science Technology and Engineering

摘　　要：研究心肌肽素对过氧化氢所致心肌细胞氧应激模型中所起的作用。采用原代培养乳鼠心肌细胞,以200μmol/L过氧化氢作用2 h诱导心肌细胞造成氧化应激模型,细胞损伤前分别给予不同浓度的心肌肽素进行干预。使用RT-PCR检测Caspase-3表达变化,MTT比色法检测原代乳鼠心肌细胞的活力,黄嘌呤/黄嘌呤氧化酶法测定超氧化物歧化酶活性。过氧化氢组心肌细胞活力低于对照组,超氧化物歧化酶活性下降(P<0.05),caspase-3 mRNA表达升高;心肌肽素组细胞活力、超氧化物歧化酶活性高于过氧化氢组,而caspase-3 mRNA表达水平较过氧化氢组降低(P<0.05),不同浓度心肌肽素之间无明显差别(P>0.05)。心肌肽素对过氧化氢造成的心肌细胞损伤作用有抵抗作用且这种抵抗作用与其抑制凋亡作用有关。To investigate if cardiomyopeptidin play roles in injured cardiomyocytes induced by hydrogen peroxide.Primary neonatal SD rat cardiac cells were treated with cardiomyopeptidin in different concentration for 24 hours and then were exposed to hydrogen dioxide for 2 hours.RT-PCR was performed to detect mRNA of Caspase-3.MTT was used for cell viability assay and superoxide dismutase（SOD） was detected.The hydrogen dioxide decreased the cell viability and SOD level while cardiomyopeptidin significantly increased both of them（P0.05）.The caspase-3 mRNA level was increased by hydrogen dioxide stress and cardiomyopeptidin treatment reduced it（P0.05）.There is no concentration dependent effect of cardiomyopeptidin in those measurement（P0.05）.Cardiomyopeptidin inhibits in vivo hydrogen dioxide induced cardiomyocytes injury and this phenomenon might be linked to its anti-apoptosis effect.

关 键 词：心肌肽素 过氧化氢 心肌细胞 

分 类 号：R963[医药卫生—微生物与生化药学]