氧化应激介导糖原合成酶激酶-3β促进肝细胞凋亡

发布时间：2018-03-04 05:06

  本文选题：氧化应激　切入点：细胞凋亡　出处：《细胞与分子免疫学杂志》2015年01期 　论文类型：期刊论文

【摘要】：目的探讨糖原合成酶激酶-3β(GSK3β)在氧化应激诱导肝细胞凋亡中的作用。方法以人肝HL-7702细胞为研究对象,H2O2/抗霉素A诱导细胞产生氧化应激,建立肝细胞凋亡模型。SB216763为GSK3β特异性抑制剂,在H2O2/抗霉素A给药前2 h干预。采用钙黄绿素乙酰甲酯/碘化丙啶(PI)双染色观察细胞存活情况,采用annexinⅤ-FITC/PI联合流式细胞术检测细胞凋亡,同时对细胞培养上清进行乳酸脱氢酶(LDH)检测来评价细胞死亡程度;Western blot法检测p-GSK3β、GSK3β、caspase-3、cleaved caspase-3、c-Jun氨基末端激酶(JNK)和细胞色素C(Cyt C)蛋白的表达。结果 H2O2/抗霉素A诱导的氧化应激促进了GSK3β活性增加,抑制GSK3β活性缓解了氧化应激和由氧化应激引起的细胞凋亡。与氧化应激模型组相比,SB216763干预组中PI染色的细胞显著减少,流式细胞术检测细胞凋亡率降低,细胞培养上清中LDH显著降低,Western blot法结果显示干预组中cleaved caspase-3、JNK、Cyt C蛋白表达下降。结论 GSK3β是氧化应激诱导细胞凋亡通路中的一种重要信号分子,抑制其活性可减轻氧化应激而改善肝细胞凋亡。
[Abstract]:Objective to investigate the role of glycogen synthase kinase 3 尾 -GSK3 尾 in oxidative stress-induced hepatocyte apoptosis. Methods Hepatocyte apoptosis model, SB216763, was established by inducing oxidative stress in human hepatic HL-7702 cells induced by H _ 2O _ 2 / anti-mycin A, and SB216763 was used as a specific inhibitor of GSK3 尾. Two hours before the administration of H _ 2O _ 2 / anti-mycin A, the cell survival was observed by double staining of calcium xanthocyanin acetyl methyl ester / pyridine iodide, and apoptosis was detected by annexin 鈪，

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