结肠炎癌转化“炎－不典型增生－癌”演进过程与“土虚-木乘-痰瘀毒结”的中医病机相契合，前期研究亦证实痛泻要方干预结肠炎癌转化有效。NF-κB/STAT3/ Wnt关键分子事件与结肠炎的恶变关系密切，而最新研究发现这一级联反应的上游，microRNA214持续过表达诱导了上述分子事件。据此提出假说：痛泻要方可能通过抑制microRNA214的持续过表达从而调控下游关键分子事件的发生发展，干预结肠炎癌转化的演进过程。本项目拟建立AOM/DSS结肠炎癌经典动物模型，采用免疫组织化学染色法、ELISA、Western Blot等检测技术，揭示痛泻要方干预结肠炎癌演进过程的生物学效应、调控途径和作用机制，阐明结肠炎癌转化的证治规律，丰富肝脾不和病机理论的内涵。

The evolution process of the transformation from colitis-associated cancer to “inflammatory-atypical hyperplasia-cancer” corresponds to TCM Pathogenesis of “deficient spleen- liver sthenia- phlegm-stasis-poisons stagnant”. Former study also proved that it is effective to induce transformation of colitis-associated cancer by Tongxieyaofang. The key molecular event of NF-κB/STAT3/Wnt is closely related to the malignant change of colitis-associated cancer. And a new research shows that this upstream of cascade reaction-sustained over-expression of microRNA214 induces above-mentioned molecular event. Based on this, a hypothesis is proposed: Tongxieyaofang regulates the occurrence and development of downstream key molecular event and intervenes the evolution process of transformation of colitis-associated cancer by inhibiting sustained over-expression of microRNA214. This project will establish an AOM/DSS colitis-associated cancer animal model by immunochemistry staining、ELISA、Western Blot，reveal biological effect、regulation pathway and mechanism of action in the evolution process of inducing transformation of colitis-associated cancer by Tongxieyaofang, illustrate the diagnosis and treatment regularity of the transformation of colitis-associated cancer，enrich the connotation of the hepatosplenic disorder pathogenesis theory .