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 Regulating ROS Level

作　　者：褚娇娇[1,2] 黄秀清[1,2] 黎健[1,2] 王抒[1,2] 

机构地区：[1]卫生部北京医院 [2]卫生部北京老年医学研究所 卫生部老年医学重点实验室,北京100730

出　　处：《现代生物医学进展》2012年第16期3001-3003,3011,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金(81070634;30801218)

摘　　要：目的: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。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 ex-pressed 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.

关 键 词：HEPG2细胞 APELIN TNF-Α 凋亡 

分 类 号：R34[医药卫生—基础医学] R593.1