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目的:观察热休克蛋白70(HSP70)在对抗氧糖剥夺中的作用和发挥抗凋亡中的分子机制，寻找HSP70发挥作用的靶点。方法:应用转染的技术将质粒和小干扰RNA(siRNA)转染入H9C2细胞内来过表达和沉默HSP70在细胞内的表达，将细胞分为对照组(control组)、缺氧复氧组(H/R组)、过表达组(H/R+HSP70)、过表达阴性对照组(H/R+NC)、沉默组(H/R+siRNA)、沉默阴性对照组[H/R+NC(siRNA)]。建立心肌细胞的缺氧复氧模型。通过细胞计数试剂盒(CCK-8)、乳酸脱氢酶(LDH)检测细胞凋亡率，通过反转录-聚合酶链反应(RT-PCR)检测B细胞淋巴瘤/白血病-2相关X蛋白(bax)、基质相互作用分子1(STIM1)的RNA表达水平。蛋白质印迹法(Western blot)检测bax、B细胞淋巴瘤/白血病-2(bcl-2)、基质相互作用分子1(STIM1)的表达，组间比较采用单因素方差分析。结果:过表达组的凋亡细胞及凋亡蛋白bax(1.97±0.01)明显低于单纯缺氧复氧组bax(2.15±0.03，n F＝356.275，n P<0.05)，差异有统计学意义，而沉默组的凋亡细胞和凋亡蛋白bax(6.09±0.17)明显高于单纯缺氧复氧组bax(2.15±0.03，n F＝356.275，n P<0.05)，差异有统计学意义；过表达组STIM1的表达量(3.14±0.14)明显低于单纯缺氧复氧组(4.46±0.20，n F＝26.602，n P<0.05)，差异有统计学意义，而沉默组STIM1的表达量(8.58±0.24)明显高于单纯缺氧复氧组(4.46±0.20，n F＝26.602，n P<0.05)，差异有统计学意义。n 结论:HSP70可能通过STIM1调节内质网钙失衡发挥抗凋亡作用。“,”Objective:To observe the role of heat shock protein 70 (HSP70) in the fight against oxygen and sugar deprivation, to explore the molecular mechanism of HSP70 in the anti-apoptosis, and to find the target of HSP70.Methods:The plasmid and siRNA were transfected into H9C2 cells to overexpress and silence the intracellular expression of HSP70 respectively. The cells were divided into control group, hypoxia and reoxygenation group (H/R group), overexpression group (H/R+ HSP70), overexpression negative control group (H/R+ NC), silence group (H/R+ siRNA) and silence negative control group [H/R+ NC (siRNA)]. The hypoxia and reoxygenation model of myocardial cells was established. Cell apoptosis rate was detected by cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH), and RNA expression levels of B cell lymphoma/leukemia-2 associated X protein (bax) and stromal interaction molecule 1 (STIM1) were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The expression of bax, B cell lymphoma/leukemia-2 (bcl-2) and stromal interaction molecule 1 (STIM1) was detected by Western blotting. One-way analysis of variance was used for comparison between groups.Results:The apoptotic cells and bax in the overexpression group were significantly lower than those (1.97±0.01 vs. 2.15±0.03, n F=356.275, n P<0.05) in the simple hypoxia and reoxygenation group, but the apoptotic cells and bax in the silence group were significantly higher than those (6.09±0.17 vs. 2.15±0.03,n F=356.275, n P<0.05) in the simple hypoxia and reoxygenation group. The expression level of STIM1 in the overexpression group was significantly lower than that in the simple hypoxia and reoxygenation group (3.14±0.14 vs. 4.46±0.20,n F=26.602, n P<0.05), and that in the silence group (8.58±0.24) was significantly higher than that in the simple hypoxia and reoxygenation group (8.58±0.24 vs. 4.46±0.20,n F=26.602, n P<0.05).n Conclusion:HSP70 exerts an anti-apoptotic effect through STIM1.