肠易激综合征（IBS）是一种消化系常见病，机制不明、缺乏有效治疗手段。其中，腹泻型IBS（IBS-D）危害最大，多因素参与发病。近期研究发现TLR4/MyD88/NF-κB信号通路介导免疫反应产生低度炎症在其发病中发挥作用，但机制不明。已有发现及课题组前期初步研究提示热休克蛋白27（HSP27）在IBS-D中高表达，另有报道阿米巴感染时HSP27抑制TLR4/MyD88/NF-κB信号通路，故推测HSP27可能通过改变TLR4/MyD88/NF-κB信号通路在IBS-D中发挥作用。故本课题拟在IBS-D大鼠中研究HSP27与TLR4/MyD88/NF-κB信号通路的变化及其相关性，通过细胞学实验探讨HSP27对该通路的作用及靶点，并在动物模型及IBS-D患者中验证相关假说及机制。本研究旨在明确HSP27对IBS-D的作用及其机制，为阐明IBS-D发病机制和寻找有效诊疗手段提供理论依据。

Irritable bowel syndrome (IBS) is a common disease of digestive system with unknown mechanism and rare effective treatment. Diarrhea-predominant irritable bowel syndrome (IBS-D) is most harmful type of IBS that many factors involved in its pathogenesis. Recent studies have found that immune response mediated by TLR4/MyD88/NF-κB signaling pathway can generate low-grade inflammation which play a role in pathogenesis of IBS-D, but the mechanism is unknown. Some results and our group's preliminary study indicate heat shock protein 27 (HSP27) high expression in IBS-D,other report finds HSP27 inhibit TLR4/MyD88/NF-κB signaling pathway in amoeba infection. So we speculate HSP27 play a role in IBS-D by changing TLR4/MyD88/NF-κB signaling pathway. Therefore, our study will observe changes of HSP27 and TLR4/MyD88/NF-κB signaling pathway and its relevance in IBS-D rats animal models, then study the effect and target of HSP27 to TLR4/MyD88/NF-κB signaling pathway by cytology test.Further,we will confirm related hypothesis and mechanisms in IBS-D rats animal models and patients with IBS-D. This study aims to find effect and mechanism of HSP27 to IBS-D and provide a theoretical basis for IBS-D in the pathogenesis, diagnosis and treatment.