热休克蛋白70对供心细胞Bcl-2、Bax蛋白表达的影响

Effects of heat shock protein 70 on myocardial expression of Bcl-2 and Bax protein of donor heart

目的探讨热休克蛋白70(HSP70)对大鼠供心心肌细胞凋亡相关基因Bcl-2、Bax蛋白表达的影响。方法Wistar大鼠18只,分为两组:对照组(C,n=9),腹腔注射生理盐水0.5ml,24h后取离体心脏灌注HTK心脏保护液,4℃保存3h后建立Langendorff离体心脏灌注模型,灌注KH液2h;实验组(E,n=9)腹腔注射重酒石酸去甲肾上腺素(溶于生理盐水中)3.1μmol/kg(0.53mg/kg),腹腔注射24h后取离体心脏,处理方法同C组。运用免疫组化SP法测定心肌HSP70含量、Bcl-2、Bax蛋白的含量以及相关生化指标并进行统计学处理。结果HSP70含量E组(17.78±1.82)较C组(5.22±1.05)明显增高(P<0.01),Bcl-2的表达E组(41.88±5.09)较C组(31.36±3.27)明显增多(P<0.01),Bax的表达E组(22.61±3.49)较C组(40.52±4.17)明显减少(P<0.01),Bcl-2/Bax比值E组(1.86±0.11)较C组(0.77±0.01)明显增高。生化指标E组明显优于C组。结论心肌HSP70高表达对供心具有明显的保护效应,其促进心肌抗凋亡蛋白Bcl-2的表达,减少促凋亡蛋白Bax表达,增加Bcl-2/Bax比率,以此抑制心肌细胞凋亡,从而发挥其对供心心肌细胞保护作用。

Objective To investigate the protection of heat shock protein 70 on donor heart and the effects on expression of myocardial cell Bcl-2 protein and Bax protein of isolated rat heart. Methods 18 Wistar rats were randomly divided into 2 groups. Controll group （C,n=9）,Normal saline 0.5 ml was injected intraperi- toneally and 24 hours later isolated hearts were stored in 4 ℃ for 3 hours with Histidine-tryptophan-ketoglutaxate （HTK） solutions, and then isolated hearts were perfusod for 2 hours by Langendorff model. Experimental group（E, n=9） ,noradrenaline bitartrate 3.1 μmol/kg（0.53 mg/kg） was injected intraperitoneally and 24 hours later isolated hearts were stored in 4 ℃ for 3＇ hours with HTK,and then isolated hearts were perfused for 2 hours with krebshenseleit （K-H） solutions by Langendorff model. Myocardial HSP70 content,the expression of Bel-2, Bax and related biochemical indicators were detected. Results HSP70,Bcl-2 in E group are higher than those in C group, Bax in E is lower than those in C and biochemical indicators in E group is better than that in C group. Conclusion This study demonstrated that the high expression of HSP70 has obvious protection on donor heart, and it can markedly affect the expression of Bcl-2,Bax of isolated rat heart,so that cardiocyle apoptosis would decrease,and it is perhaps one of important factors for myocardial protection.