文章摘要
庞斯斯,张小进,姜苏蓉,刘 莉,程蕴琳.Akt参与热休克蛋白27保护大鼠心肌细胞过氧化损伤[J].南京医科大学学报,2008,28(5):613~617
Akt参与热休克蛋白27保护大鼠心肌细胞过氧化损伤
Akt is involved in the cytoprotection of Heat shock protein27 from H2O2-induced damage in rat cardiac cells
投稿时间:2007-12-14  
DOI:10.7655
中文关键词: 热休克蛋白27  Akt  氧化应激
英文关键词: heat shock protein27  Akt  oxidative stress
基金项目:江苏省卫生厅"十一五兴卫工程/老年医学重点学科"专项基金,江苏省科技厅自然科学基金(BK2007247),教育部博士点专项基金(20050312008)
作者单位
庞斯斯 南京医科大学第一附属医院老年医学科,江苏 南京 210029 
张小进  
姜苏蓉  
刘 莉  
程蕴琳  
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中文摘要:
      目的:探讨小分子热休克蛋白27保护大鼠心肌细胞过氧化损伤的机制?方法:①以稳定转染pCDNA3.1/Hsp27质粒并稳定高表达Hsp27的大鼠心肌细胞株H9c2(H9c2-Hsp27)为研究对象,对照组采用稳定转染pCDNA3.1质粒的H9c2(H9c2-Vector)细胞;②氧化应激诱导和检测:500 ?滋mol/L H2O2处理细胞后进行如下分析:培养上清中的LDH活性?细胞形态学改变?细胞内Akt激活水平;③Akt在Hsp27保护H2O2诱导H9c2 损伤中的作用:以Akt抑制剂Triciribine处理H9c2-Hsp27,观察其对Hsp27保护H2O2诱导H9c2 形态学变化的影响?结果:①H2O2诱导H9c2细胞向培养上清释放的LDH显著增加(P < 0.01),但与对照组相比,Hsp27高表达显著抑制了H2O2诱导的LDH释放(P < 0.01);②H2O2处理后,H9c2细胞Akt磷酸化水平增加(P < 0.01或P < 0.05),但与H9c2-Vector比较,H9c2-Hsp27的Akt磷酸化水平进一步增强(P < 0.05);③Akt磷酸化被抑制后,Hsp27对H2O2 诱导H9c2细胞形态学改变的保护作用消失?结论:Akt激活是Hsp27保护大鼠心肌细胞过氧化损伤的重要机制?
英文摘要:
      Objective:To investigate the mechanisms of the cytoprotection of Heat shock protein27(Hsp27) from H2O2-induced damage in rat cardiac cells. Methods:①Rat cardiac cell line H9c2 with stable overexpression of Hsp27(H9c2-Hsp27) was used in the experiment,empty vector transfected H9c2(H9c2-Vector) served as control;②Oxidative stress induction and analysis:Cells were treated with 500 ?滋mol/L H2O2 and underwent the following examination:LDH activity in culture medium,cell morphology and intracellular Akt activation;③Role of Akt in the protection of Hsp27 from oxidative damage in H9c2:Triciribine,a selective inhibitor of AKT phosphorylation,was introduced in the culture. After pre-treated with Triciribine,H9c2-Hsp27 cells were incubated with 500 ?滋mol/L,then the morphology was observed. Results:①H2O2 induced LDH releasing significantly increased in the culture medium both in H9c2-Vector and H9c2-Hsp27(P < 0.01). However,compared with H9c2-Vector controls,H2O2 induced LDH release was significantly attenuated in H9c2-Hsp27(P < 0.01);②H2O2-induced Akt phosphorilation was augmented by Hsp27 overexpression in H9c2-Hsp27,in comparison with H9c2-Vector(P < 0.05);③After Akt phosphorylation was inhibited,the protection of Hsp27 from H2O2 in cell morphology was disappear. Conclusion:Akt activation is involved in the cytoprotection of Hsp27 from oxidative damage in rat cardiac cells.
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