溃疡性结肠炎（UC）以慢性、反复发作的结肠粘膜炎症与溃疡为特点，严重影响患者的生活质量，还有很高的癌变风险。UC发病机制尚不完全明确，但已证实肠上皮通透性增加在UC发病机制中起重要作用。多数与EP增加相关的研究都集中在上皮屏障完整性方面。一项最新的研究证实结肠粘膜血管内皮损伤导致粘膜血管通透性（VP）增加早于结肠上皮功能改变和肠粘膜损伤，可能是引起UC的始动因素。但VP月EP之间的关系尚不明确。我们推测VP增加可能是另一条由内向外的引起EP增加的重要途径，本研究通过对UC发病过程中VP和EP变化及调节因子的动态观察，进一步明确VP增加在UC发病机制中的作用，从而为中医理论"行血则便脓自愈"提供科学依据。并在此基础上研究清肠栓调节VP的药理作用及相关机制。

Ulcerative colitis (UC) is characterized by chronic, recurrent ulcers and inflammation of the colonic mucosa. UC seriously influenced the quality of life in patients. Morover, people who have UC are at an increased risk of developing cancer. Although the pathogenesis of UC is not fully understood, the increased epithelial permeability(EP)has been shown to play important pathophysiologic role. Most publications on the role of intestinal permeability mostly focus on disrupted epithelial barrier integrity in the pathogenesis of UC.A more recent study demonstrated that endothelial damageand increased colonicvascular permeability(VP) precede the changes in colonicepithelial barrier function and the development of colonic lesions，might be a critical early step in disease pathogenesis。But the relation beteween increased VP and increased EP is still unclear. We suppose that increased VP is an important intermediate factor to induce the increase of EP. In this study,we will observe the dynamic change pf VP and EP with their mediators during the course of UC and identify the pathogenic role of VP in the development of UC.Based on this,we will investigate the pharmacological effect on VP and the mechanisms involved.