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热休克预处理对大鼠心肌细胞凋亡和金属硫蛋白表达的影响 被引量:1

Effects of heat shock pretreatment on rat myocardial apoptosis and mitochondrial metallothionein expression
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摘要 目的:探讨热休克预处理对大鼠心肌细胞凋亡和金属硫蛋白表达的影响。方法:将体外培养的大鼠心肌细胞随机分为3组:对照组(C组)、H2O2损伤组和热休克预处理组,检测心肌细胞的凋亡、心肌细胞Caspase-3活性,并用Western blotting检测线粒体中细胞色素C和金属硫蛋白的表达。结果:与对照组相比,H2O2损伤组心肌细胞凋亡数目增加(P<0.01),Caspase-3活性明显增高(P<0.01),线粒体中细胞色素C和金属硫蛋白的蛋白表达量明显增高(P<0.01),而给予热休克预处理的心肌细胞的凋亡数量和坏死细胞数较H2O2损伤组明显下降(P<0.01),参与细胞凋亡执行的Caspase-3活性明显降低(P<0.01),细胞色素C和金属硫蛋白的蛋白表达量持续升高(P<0.01)。结论 :热休克预处理能够抑制心肌细胞凋亡,增加对心肌起保护作用的金属硫蛋白的表达,减少线粒体细胞色素C的释放,从而对心肌细胞起保护性作用。 Objective= To investigate the effects of heat shock pretreatment on rat myocardial apoptosis induced by hy- drogen peroxide(H2 02 ) and the mitochondrial metallothionein expression. Methods:The cells cultured in vitro were randomly divided into 3 groups(n= 6), control group, H2 O2 injury group and heat shock pretreatment group. The apoptosis of myocardi- al cells, myocardial cells Caspase 3 activity and mitochondrial cytochrome C and the expression of metallothionein were meas- ured. Results:Compared with control group, increased number of myocardial cell apoptosis (P〈0.01), significantly increased Caspase 3 activity (P〈0.01), significantly higher protein expression of mitochondrial eytoehrome C and metallothionein pro- tein (P〈0.01) were observed in the H2Oz injury group. Compared with H202 injury group, pretreatment with heat shock group, the number of the apoptosis of myocardial cells and necrotic cells was significantly lower (P〈0.01), Caspase 3 activity were significantly decreased (P〈0. 01), significantly higher protein expression of mitochondrial cytochrome C and metallothio- nein protein were found. Oonclusions:Heat shock pretreatment can inhibit myocardial apoptosis, increase the myocardial pro- tection of metallothionein expression, reduce the release of mitochondrial cytochrome C, and has protective effects on myocar- dial cells.
作者 於建鹏 唐菲
出处 《海南医学院学报》 CAS 2015年第5期600-603,共4页 Journal of Hainan Medical University
基金 黄石市科技局(2012D130001000070)~~
关键词 热休克预处理 心肌细胞 金属硫蛋白 H2O2损伤 凋亡 细胞色素C Heat shock pretreatment Myocardial cells metallothionein H2 O2 injury Apoptosis Cytochrome C
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