文章摘要
褚娇娇黄秀清黎健王抒.Apelin 通过调节ROS 水平抑制TNF-α 诱导的HepG2 细胞凋亡[J].,2012,12(16):3001-3003
Apelin 通过调节ROS 水平抑制TNF-α 诱导的HepG2 细胞凋亡
Apelin Inhibits TNF-α-Induced HepG2 Cell Apoptosis by RegulatingROS Level
  
DOI:
中文关键词: HepG2 细胞  Apelin  TNF-α  凋亡
英文关键词: HepG2 cells  Apelin  TNF-α  Apoptosis
基金项目:国家自然科学基金(81070634,30801218)
作者单位
褚娇娇黄秀清黎健王抒 卫生部北京医院/ 卫生部北京老年医学研究所卫生部老年医学重点实验室 
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中文摘要:
      探讨apelin 在肿瘤坏死因子(tumor necrosis factor-α, TNF-α)诱导的肝细胞凋亡中的作用及可能机制。方法:PCR 检测 HepG2 细胞和原代小鼠肝细胞中APJ 受体的表达;采用Hoechst 33342 染色检测TNF-α 诱导的HepG2 细胞凋亡;用活性氧 (ROS)检测试剂盒结合流式细胞术测定细胞内ROS 水平;通过Western blot 检测信号分子JNK 的磷酸化水平;比较给予apelin 处理对上述指标的影响。结果:HepG2 细胞和原代小鼠肝细胞均表达APJ 受体;apelin 可抑制TNF-α 导致的细胞内ROS 生成增 多和JNK 磷酸化水平升高并减少TNF-α 诱导的HepG2 细胞凋亡。结论:Apelin 可能通过拮抗TNF-α 诱导的细胞内ROS 水平升 高,使JNK 信号失活,从而抑制HepG2 细胞凋亡。
英文摘要:
      Objective: To investigate the effect of apelin on TNF-α-induced apoptosis of HepG2 cells. Methods: HepG2 cells were treated with TNF-α to induce apoptosis. The expression of APJ receptor in HepG2 cells and primary mouse hepatocytes was detected by RT-PCR. Hoechst 33342 staining was performed to analyze the apoptosis of HepG2 cells. Intracellular ROS levels were measured by ROS detection kit combined with flow cytometry. Phosphorylation of JNK was detected through Western blot. Results: APJ receptor expressed in HepG2 cells and primary hepatocytes. In the TNF-α treated HepG2 cell, JNK phosphorylation was activated, the level of ROS increased and cell apoptosis was induced. However, apelin treatment significantly decreased JNK phosphorylation and ROS level, and protected cells from apoptosis. Conclusion: Apelin may protect HepG2 cells from TNF-α-induced apoptosis by reducing intracellular ROS level and inactivating JNK signaling.
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