恩替卡韦对肝癌HepG2细胞凋亡的诱导作用及其机制
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篇名: 恩替卡韦对肝癌HepG2细胞凋亡的诱导作用及其机制
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摘要: 目的:研究恩替卡韦对肝癌HepG2细胞凋亡的诱导作用及其机制。方法:以0(正常对照组)和10、30、100 μmol/L(低、中、高浓度组)恩替卡韦作用于HepG2细胞48 h,采用MTT法检测细胞活力;膜联蛋白Ⅴ(Annexin Ⅴ)-碘化丙啶(PI)流式双染法检测细胞凋亡情况;Western blot法检测细胞中核因子-κB p65(NF-κB p65)和核因子-κB抑制因子α(IκBα)磷酸化水平,以及Bax、Bcl-2、生存素及C-myc蛋白表达。结果:与正常对照组比较,恩替卡韦低、中、高浓度组细胞活力,NF-κB p65、IκBα磷酸化水平,Bcl-2、生存素及C-myc蛋白表达均降低,细胞凋亡率、Bax蛋白表达均升高(P<0.05或P<0.01),且呈浓度依赖性。结论:恩替卡韦能降低HepG2肝癌细胞的活力并诱导其凋亡,其机制可能与上调Bax表达,下调Bcl-2、生存素、C-myc表达及抑制NF-κB/IκBα信号通路激活有关。
ABSTRACT: OBJECTIVE: To study induction effect of entecavir on the apoptosis of hepatocellular carcinoma HepG2 cells and its mechanism. METHODS: After treated with 0 (normal control), 10, 30 and 100 μmol/L (low, medium and high concentration groups) entecavir for 48 h, MTT method was adopted to detect HepG2 cell viability. AnnexinⅤ-PI flow double staining was used to detect cell apoptosis. Western blot was used to determine the phosphorylation of nuclear factor kappa B p65 (NF-κB p65) and nuclear factor kappa B inhibitor α (IκBα), and the protein expression of Bax, Bcl-2, Survivin and C-myc.  RESULTS: Compared with normal control group, the cell viability, the phosphorylation of NF-κB p65 and IκBα, and the protein expression of Survivin, C-myc and Bcl-2 of entecavir low, medium and high concentration groups all decreased; the apoptotic rate, the protein expression of Bax increased (P<0.05 or P<0.01), in concentration-dependent manner. CONCLUSIONS: Entecavir can decrease viability of HepG2 cells and induce cell apoptosis, which is related to up-regulation expression of Bax, down-regulation expression of Survivin, C-myc and Bcl-2, and blocking the activation of NF-κB/IκBα signaling pathway.
期刊: 2016年第27卷第10期
作者: 张玉山
AUTHORS: ZHANG Yushan
关键字: 恩替卡韦;肝癌HepG2细胞;凋亡;机制
KEYWORDS: Entecavir; Hepatocellular carcinoma HepG2 cells; Apoptosis; Mechanism
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