UC肠纤维化是结肠长期慢性炎症的结果，其主要特征为损伤与修复异常导致的间质纤维组织过度增生。自噬通过调节细胞修复或死亡在UC肠纤维化的损伤与修复过程中发挥重要作用。TGF-β1在UC的发病过程中调节自噬过程影响UC肠纤维化进展，Snail是UC肠纤维化进程中同样发挥枢纽作用的另一个关键性调控因子。我们前期研究发现，湿生扁蕾提取物可抑制大鼠UC肠纤维化程度并减少TGF-β1表达，可调控自噬相关蛋白ATG16L1和LC3及EMT表型蛋白E-cadherin和α-SMA的表达，但机制尚不清楚。我们推测“湿生扁蕾提取物可能通过TGF-β1/Smads/Snail信号通路调控CEC自噬障碍导致的EMT发挥其治疗UC肠纤维化作用”。为证实该假说，我们拟在体外建立CEC自噬障碍模型及大鼠UC肠纤维化模型，探讨湿生扁蕾提取物对UC肠纤维化的治疗作用及可能的机制，以期为UC肠纤维化治疗提供新思路和新方法。

Ulcerative colitis fibrosis is the result of long-term chronic inflammation of the colon, with the main features of interstitial fibrous tissue hyperplasia due to injury and repair abnormalities. Autophagy plays an important role in the process of injury and repair of colonic fibrosis by regulating cell repair or death. TGF-β1 could regulate autophagy during the occurrence of ulcerative colitis and affects the progression of colonic fibrosis. Snail is another pivotal regulator that also plays a pivotal role during the process of colonic fibrosis. Our previous study found that Gentianopsis paludosa extract could significantly inhibit UC rat intestinal fibrosis and reduce TGF-β1 expression, regulate the expression of autophagy-related proteins ATG16L1, LC3, adjust and control EMT phenotype proteins E-cadherin and α-SMA, but the mechanism was unclear. We speculate that Gentianopsis paludosa extract may play a crucial role in the treatment of UC intestinal fibrosis by acting on TGF-β1/Smads /Snail signaling pathway and regulating autophagy disorders of CEC cells leading to EMT. To confirm this hypothesis, we intend to establish a model of autophagy in CEC cells in vitro and UC rat model of intestinal fibrosis. Therapeutic effect and its possible mechanism of Gentianopsis paludosa extract on UC intestine fibrosis would be explored in order to provide new strategy and new methods for the treatment of UC intestinal fibrosis.