溃疡性结肠炎(UC)是肠道黏膜反复炎症与免疫失衡的共同结果。研究表明，IL-6-STAT3/SOCS1信号交互调控UC的炎症与免疫耐受，而miR155是该信号通路上游调控的关键因子。前期临床运用溃结宁膏穴位敷贴治疗“虚、瘀”UC取得显著疗效，其机制是减少促炎因子的释放和抑制免疫的过度激活。因此，我们推测溃结宁膏穴位敷贴可能在炎症信号通路的上游就发挥调控作用，即通过miR155-IL-6-STAT3/SOCS1信号交互调控UC炎症与免疫耐受。本课题拟建立“虚、瘀”状态UC动物模型及体外HT-29炎症细胞培养，采用流式细胞、免疫组化、Western Blot、RT-PCR、免疫共沉淀等技术检测miR155-IL-6- STAT3/SOCS1通路的关键基因与蛋白表达，探讨miR155调控该信号通路的交互作用而介导UC炎症与免疫平衡的分子机制，为揭示溃结宁膏穴位敷贴治疗UC的作用靶点提供客观依据。

Ulcerative colitis (UC) is a common result of repeated intestinal inflammatory response and immune imbalance.The study showed that IL-6-STAT3 / SOCS1 signal interacts with UC's inflammation and immune tolerance, while miR155 is a key factor in the upstream regulation of this signaling pathway.Early clinical application of Kui Jie Ning Plaster point application treatment of spleen and kidney yang deficiency type UC achieved significant effect, the mechanism is to reduce the release of proinflammatory factors and inhibit the immune over-activation.Therefore, we speculate that the Kui Jie Ning Plaster point application may play an regulatory role in the upstream of the inflammatory signaling pathway, that is, through the miR155-IL-6-STAT3/SOCS1 signal to regulate UC inflammation and immune tolerance.In the study, we establish “deficiency and stasis”UC animal model and culture HT-29 Inflammatory cell in vitro.The key genes and protein expression of miR155-IL-6-STAT3 / SOCS1 pathway were detected by flow cytometry, immunohistochemistry, Western Blot, RT-PCR and immunoprecipitation explore the molecular mechanism of miR155 regulating the interaction of UC signaling and mediating UC,to provide an objective basis for revealing the target of the treatment of UC by Kui Jie Ning Plaster point application.