PTD4-Cu/Zn SOD融合蛋白对大鼠心肌细胞缺氧复氧损伤的影响-现代医学

PTD4-Cu/Zn SOD融合蛋白对大鼠心肌细胞缺氧复氧损伤的影响

单位：十堰市太和医院(湖北医药学院附属医院)麻醉科, 湖北十堰 442000

分类号：R-33;R364.4

出版年·卷·期（页码）：2017·36·第十期（1396-1399）

摘要：

目的：评价细胞穿透肽4即蛋白转导结构域4（PTD4）介导的铜锌超氧化物歧化酶（Cu/Zn SOD）对大鼠心肌细胞缺氧复氧损伤（HRI）的影响。方法：用厌氧（85% N₂、10% H₂、5% CO₂）培养箱制作大鼠心肌细胞（H9C2）HRI模型，设置HRI组（HRI的细胞培养液中不加任何处理因素）、HRI+Cu/Zn SOD组（加入10 μmol·L^-1 Cu/Zn SOD）、HRI+PTD4-Cu/Zn SOD组（10 μmol·L^-1 PTD4-Cu/Zn SOD），另外以正常培养心肌细胞作为正常对照组，孵育30 min后，末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）技术检测心肌细胞凋亡，蛋白印迹法检测心肌细胞Bcl-2、Bax蛋白的表达。结果：HRI+PTD4-Cu/Zn SOD组心肌细胞凋亡指数[（10.20±2.77）%]比HRI组[（28.40±2.41）%]明显降低，与HRI组比较，HRI+PTD4-Cu/Zn SOD融合蛋白能显著增加Bcl-2蛋白表达，降低Bax蛋白表达。结论：PTD4-Cu/Zn SOD融合蛋白可以减轻大鼠心肌细胞的HRI。

Objective: To investigate whether the cell-penetrating peptide, protein transduction domain 4(PTD4) mediates the protective effects of copper-zinc superoxide dismutase (Cu/Zn SOD) on hypoxia/reoxygenation injury(HRI) in rat myocardial cells.Methods: Myocardial cell H9C2 cultured in vitro were randomized into 4 groups:normal group, HRI group, HRI-treated H9C2 cells with Cu/Zn SOD(HRI+Cu/Zn SOD group), HRI-treated H9C2 cells with PTD4 and Cu/Zn SOD(HRI+PTD4-Cu/Zn SOD group). HRI was achieved by exposing cardiomyocytes to 4 h hypoxia followed by 2 h reoxygenation. Cardiomyocyte apoptotic index,Bax and Bcl-2 in cardiomyocytes were detected with TUNEL and Western blot. Results: HRI+PTD4-Cu/Zn SOD reduced apoptosis of cardiomyocytes induced by hypoxia/reoxygenation injury. Compared with HRI group,HRI+PTD4-Cu/Zn SOD group significantly reduced the expression of Bax and increase the expression of Bcl-2.Conclusion: Cu/Zn SOD mediated by cell penetrating peptide PTD4 can attenuate hypoxia/reoxygenation injury in rat myocardial cells.

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