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目的观察低温联合还原型谷胱甘肽对缺血-再灌注诱导的L02肝细胞凋亡的影响,并探索相关分子机制。方法MTT比色法检测低温联合还原型谷胱甘肽对细胞活力的影响;试剂盒检测低温联合还原型谷胱甘肽对细胞丙二醛(MDA)水平、乳酸脱氢酶(LDH)释放及超氧化物歧化酶(SOD)活力的影响;激光共聚焦显微镜检测细胞内活性氧簇(ROS)生成;Western blot法检测低温联合还原型谷胱甘肽对bcl-2及bax蛋白表达水平的影响。结果低温联合还原型谷胱甘肽能明显抑制缺血-再灌注诱导的L02肝细胞活力降低(P<0.05);低温联合还原型谷胱甘肽处理细胞能明显抑制缺血-再灌注诱导的L02肝细胞MDA生成增加、LDH水平增高及SOD活力降低(P<0.05);低温联合还原型谷胱甘肽处理细胞能明显抑制缺血-再灌注诱导的L02肝细胞内bcl-2蛋白表达水平降低及bax蛋白表达水平增高(P<0.05)。结论低温联合还原型谷胱甘肽可能通过上调bcl-2的表达及下调bax的表达抑制缺血-再灌注诱导的L02肝细胞凋亡发生。
Objective To observe the effects of low-temperature combined with reduced glutathione (GSH-Px) on the apoptosis of L02 hepatocytes induced by ischemia-reperfusion and explore the related molecular mechanisms. Methods MTT assay was used to detect the effects of low-temperature combined with reduced glutathione (GSH) on cell viability. The kit was used to detect the effects of low-temperature combined with reduced glutathione (GSH) on malondialdehyde (MDA), lactate dehydrogenase (LDH) The effect of low temperature combined with reduced glutathione on the expression of bcl-2 and bax protein was examined by laser scanning confocal microscopy. . Results Low-temperature combined with reduced glutathione (GSH-Px) could significantly inhibit the decrease of L02 hepatocyte viability induced by ischemia-reperfusion (P <0.05). Low temperature combined with reduced glutathione could significantly inhibit ischemia-reperfusion- L02 hepatocytes MDA increased, LDH levels increased and SOD activity decreased (P <0.05); low temperature combined with reduced glutathione treatment of cells can significantly inhibit ischemia-reperfusion-induced L02 hepatocytes bcl-2 protein expression levels Decreased and the expression of bax protein increased (P <0.05). Conclusion Low-temperature combined with reduced glutathione may inhibit the apoptosis of L02 hepatocytes induced by ischemia-reperfusion through up-regulating the expression of bcl-2 and down-regulating the expression of bax.