热休克蛋白72在氧化应激所致急性乳鼠培养心肌细胞损伤中的作用  

Effect of HSP72 on acute injury of neonatal cardiomyocytes induced by oxidative stress

作　　者：罗学滨[1] 刘可[2] 易宇欣[2] 王浩[2] 刘梅冬[2] 肖献忠[2] 邓恭华[2] 

机构地区：[1]中南大学湘雅医学院中心实验室,长沙410078 [2]中南大学湘雅医学院病理生理学教研室,长沙410078

出　　处：《中南大学学报（医学版）》2006年第2期228-231,共4页Journal of Central South University ：Medical Science

摘　　要：目的:探讨HSP7 2对氧化应激所致心肌细胞急性损伤的保护作用。方法:用热休克预处理诱导新生大鼠心肌细胞中HSP7 2的表达,采用HSP7 2反义寡核苷酸阻断HSP7 2的表达。向原代培养的乳鼠心肌细胞中加入终浓度为0.5 mmol/L H2O2,以模拟氧化应激。测定乳酸脱氢酶释放率和细胞总蛋白质合成能力。结果:氧化应激引起心肌细胞乳酸脱氢酶释放率明显升高,而细胞总蛋白质的合成降低。热休克预处理导致心肌细胞中HSP7 2表达明显增加,并使H2O2所致心肌细胞LDH释放率显著降低,细胞总蛋白质的合成基本恢复正常水平。HSP7 2反义寡核苷酸能在很大程度上阻断HSP7 2的表达及热休克预处理所所致的心肌细胞保护作用。结论:在热休克预处理减轻过氧化氢所致乳鼠心肌细胞急性损伤的作用中,HSP7 2发挥了主要作用。Objective To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress. Methods Cardiomyocytes of neonatal rats treated with heat shock （42 ℃, 30 min, recovery for 6 h ） to induce the expression of HSP72 and HSP72 antisense oligonueleotide was transformed to block the expression of HSP72. 0. 5 mmol/L （final concentration ） H2 O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyoeytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats. Results Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP72 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2. Conclusion HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.

关 键 词：热休克蛋白72 反义寡核苷酸 心肌细胞 氧化应激 

分 类 号：R363[医药卫生—病理学]