基于ERK1/NLRP3信号通路介导外泌体miRNA-155探讨安肠汤防治IBS-D炎症机制的研究

IBS-D的发病机制一直是功能性胃肠病的研究热点，如何提高内脏疼痛阈值是治疗此病的关键之一。前期研究示ERK1等与疼痛敏感化相关的因子表达与肠道诸多炎症因子密切相关，且安肠汤可通过改善炎症状态来降低疼痛相关因子表达。大量文献显示NLRP3炎症小体是这些炎症因子的释放加速器，而miRNA-155可搭乘体内的外泌体通过ERK1途径参与NLRP3炎症小体活动。预实验显示安肠汤可降低模型组大鼠血液中外泌体的数量。综上推测安肠汤可通过抑制外泌体或外泌体miRNA-155的表达，降低ERK1/NLRP3信号通路活性，达到调控炎症因子缓解腹痛的目的。本课题应用超速离心法、Real-timePCR、ELISA、透射电镜等，通过应激-束缚联合辣椒素灌胃构建大鼠IBS-D模型，体外细胞炎症模型，探讨安肠汤如何调控外泌体及miRNA-155的表达，减少炎症因子的释放，达到防治IBS-D的科学依据，造福广大患者。

The pathogenesis of IBS-D has been a research hotspot in functional gastrointestional diseasea.How to raise the threshold of visceral pain is one of the key factors in treating this disease.Early studies have shown that the expression of ERK1 and other factors related to pain sensitivity is closely related to many inflammatory factors in the intesttine,And Anchang decoction can reduce the expression of pain related factors by improving the inflammatory state.Numerous literatures show that NLRP3 inflammasome is the release accelerator of these inflammatory factors,and miRNA-155 can take the Exosome in vivo to participate in NLRP3 inflammasome activity through ERK1 pathway.Pre-experiment shows that Anchang decoction can reduce the amout of Exosome in the blood of rats in the model group,To sum up,it,is speculated that Anchang decoction can reduce the activity of ERK1/NLRP3 inflammasome signaling pathway and achieve the purpose og regulating inflammatory factors to relieve abdominal pain by inhibiting the expression of Exosome or regulating the expression of Exosome mirna-155.In this study,we will construct the rate IBS-D model by stress binding combined with capsaicin perfusion and construct in vitro cell inflammatory model to explore the scientific basis of the Anchang decoction for the prevention and treatment of IBS-D fof the benefit of the majority of patients,by regulating the expression of Exosome,and reducing the release of inflammatory factors.Ultracentrifugation、Real-time PCR、ELISA、transmission election microscope and other techniques will be appled.