Jagged1蛋白对乳鼠心肌细胞缺氧复氧损伤的作用

目的研究Jagged1蛋白（Ja1）对乳鼠心肌细胞缺氧复氧损伤（SI/RI）的作用,为探明Notch信号通路在心肌缺血再灌注损伤（I/RI）中的作用提供理论依据。方法实验分为5组,分别为正常对照组、SI/RI组、缺氧复氧＋不同浓度Ja1组（5、10、20μM）,四氮唑盐比色（MTT）法测定各组细胞存活率;缺口末端标记（TUNEL）法测定各组细胞凋亡率;专用试剂盒检测培养液中超氧化物歧化酶（SOD）、丙二醛（MDA）含量。结果与对照组相比,SI/RI组细胞活力明显下降（P〈0.01）,凋亡率明显上升（P〈0.01）,同时期培养液中SOD水平明显降低（P〈0.01）,MDA水平显著升高（P〈0.01）;不同浓度Ja1可以使上述指标明显改善（P〈0.01）,并呈浓度依赖性。结论 Ja1蛋白对SI/RI造成的心肌细胞损伤具有保护作用,作用机制与增强细胞抗凋亡、抗氧化以及减轻脂质过氧化物导致的细胞膜损伤有关,Notch信号通路可能在心肌缺血再灌注损伤中发挥重要的调控作用。

Effects of Jagged1 protein on neonatal rat cardiomyocytes induced by simulated ischemia reperfusion injury

Objective To investigate the effects of Jagged1 protein （Jal） on neonatal rat cardiomyocytes induced by simulated ischemia reperfusion injury （SI/RI）, and to explore the role of Notch signaling pathway in myocardial ischemia reperfusion injury （L/ RI）. Methods The cardiomyocytes were divided into 5 groups： Control, SL/RI, SL/RI ＋Jal （5, 10, 20 μM）. MTT method used to determin the survival rate of cells; TUNEL used to detect the apoptotic rate of cells; The special kits were used to detect the levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in the culture medium. Results Comparing with the Control group, the cell survival rate in the SI/RI group decreased significantly, and the apoptotic rate increased significantly, while the SOD level in the culture medium decreased significantly, and the MDA level increased significantly. The above parameters of cells were improved signif- icantly when treated by Jal on concentration - dependent manner. Conclusion Jaggedl protein has the protective effect on the neonatal rat cardiomyocytes induced by SI/RI, this special mechanisms includes： anti- oxidation, anti- apoptosis, and alleviate the cell mem- brane damage induced by lipid peroxides. Notch signaling pathway may play a vital regulatory role in the myocardial reperfusion injury.