非酒精性脂肪性肝炎 (NASH) 发病率逐年上升，严重危害人类健康，目前仍缺乏有效干预措施。有研究显示，TLR4活化释放大量炎性因子和代谢紊乱诱导的内质网应激 (ERS) 反应是启动NASH的重要因素。新近研究发现，ERS通过放大TLR4信号通路增加炎性因子释放是炎症性疾病的关键环节。我们前期研究发现，竹节参总皂苷通过抑制炎性因子表达能有效干预NASH进程；预实验结果显示，竹节参总皂苷可调控ERS信号分子GRP78和CHOP，抑制TNF-α和IL-1β的表达，提示竹节参总皂苷可能通过干预ERS信号分子，进而阻断ERS对TLR4信号的放大效应，干预NASH的肝脏炎症反应。基于此，我们应用高脂诱导NASH模型，采用重组病毒、免疫荧光、siRNA等技术，研究竹节参总皂苷干预NASH炎症反应的分子机制是否与ERS信号分子介导的TLR4炎症信号放大效应密切相关，为NASH的防治提供新思路和新靶点。

In recent years the increasing prevalence of Non-alcoholic steatohepatitis (NASH) has caused serious harm to human health in China. There is still a lack of effective intervention strategy for the NASH. The research showed that the TLR4 signaling activation to release lots of inflammatory factors and the disorder of lipid metabolism induced endoplasmic reticulum stress (ERS) are acknowledged as having an important role in initiating NASH. ERS sensitizes TLR4 signal pathway to increase production of inflammatory cytokines is the newly discovered key factor for the inflammatory diseases. Our previous study found that total saponins of Panax japonicus effectively prevented NASH process through inhibition of the inflammatory reaction. The pre-experiment results showed that Panax japonicus saponins regulated the ERS signal molecular GRP78 and CHOP, and inhibited TNF-α and IL-1β cytokine expression. These experimental results suggest that total saponins of Panax japonicus may prevent the inflammation of NASH through the intervention of ERS signaling molecules to TLR4 signal pathway. Based on the hypothesis, the effect of total saponins of Panax japonicus on the prevention of NASH will be studied in the high fat induced NASH model. Using recombinant virus, immunofluorescence, and siRNA techniques, the molecular mechanism of total saponins of Panax japonicus will be investigated on the regulation of ERS signaling molecules which amplifies TLR4 inflammatory signaling. This research will provide new ideas and new targets for the prevention and treatment of NASH.