中文摘要：

目的：研究TLR4信号通路活化对 polyI：C诱导人肝癌细胞系H7402凋亡的影响,并分析其可能的作用机制.方法：用TLR4激动剂LPS处理H7402细胞 24 h后,转染polyI：C刺激24 h,然后利用流式细胞术检测细胞凋亡,荧光定量PCR检测凋亡基因及胞内RNA模式识别受体TLR3、MDA5、RIG-I和LGP2的表达,Western blot检测识别受体的蛋白表达水平.结果：LPS预处理,减弱了polyI：C诱导H7402细胞凋亡的作用.同时,促凋亡基因Noxa的表达水平降低.在此过程中polyI：C的胞内识别受体RIG-I、MDA5的基因和蛋白水平表达下调.结论：LPS可能通过降低H7402细胞内dsRNA识别受体的表达,抑制了polyI：C诱导H7402细胞凋亡的作用.

英文摘要：

Objective：To investigate the influence of TLR4 signaling activation on polyI：C-induced apoptosis of H7402 cells and the mechanisms involved in this process. Methods： After pre-treatment with TLR4 ligand LPS for 24h, polyI ： C was transfected into H7402 cells. After an additional 24hs, FACS was used to evaluate the apoptosis rate, and real-time quantitive PCR was performed to analyze the expression of apoptotic genes and RNA-sensing pattern recognition receptors （PRRs） , including TLR3, MDA5, RIG-I and LGP2. The protein level of MDA5 and RIG-I was measured by Western blot. Results： LPS pre-treatment could inhibit polyI：C-induced the apoptosis of H7402 cells. Further research showed that the expression of RIG-I, MDA5 as well as the pro-apoptotic gene Noxa was decreased in the process. Conclusion： LPS pre-treatment lead to the reduction of intracellular RNA-sensing PRRs, and then inhibite polyI：C-induced the apoptosis of H7402 cells.