炎症性肠病（IBD）的病因和发病机制仍不清楚。文献及我们的前期研究证实肠神经系统（ENS）在IBD发病中起重要作用。本研究继续从ENS入手，但以肠神经胶质细胞（EGC）和肠平滑肌细胞（ISMC）为突破口。采用EGC培养上清液腹腔注射和GDNF（+/-）杂合子小鼠以及GDNF重组腺病毒灌肠野生Balc/C小鼠，造成EGC分泌增加和GDNF缺乏和/或增加的体内背景，并构建葡聚糖硫酸钠（DSS）及三硝基苯磺酸（TNBS）结肠炎模型，在此基础上使用ISMC的激动剂/拮抗剂，从动物水平探讨EGC及其分泌的GDNF对ISMC的影响以及在IBD发病中的作用；以EGC培养上清液体外培养ISMC，在细胞水平研究EGC对ISMC的影响；采用免疫印迹等技术从分子水平探讨GDNF/GFRa1/RET通路在两细胞功能发挥及IBD发病中的作用及机制。旨在从ENS角度阐明IBD的发病机制，为IBD防治奠定理论基础。

The etiology and pathogenesis of inflammatory bowel disease (IBD) are still unclear. As reported from prior literature and our previous study, enteric nerve system (ENS) plays an important role in the pathogenesis of IBD. This project focuses on the effects of enteric glial cell (EGC) and its glial cell line-derived neurotrophic factor (GDNF) on intestinal smooth muscle cell (ISMC) and its role on the pathogenesis of IBD. In animal experiment, ISMC agonist or antagonist were added to GDNF (+/-) heterozygous mice with GDNF partially knocked out or wild type mice treated with Ad-GDNF enema, to examine the effects of EGC and its GDNF on ISMC and its role in the pathogenesis of IBD. The effects of EGC on ISMC were investigated at a molecular level by culturing ISMC in EGC culture supernatant. Such methods as western blot were used to analyze the effects of GDNF/GFRa1/RET signaling pathway in the function of EGC and ISMC and the pathogenesis of IBD. This study contributes to illuminating the pathogenesis of IBD from the perspective of ENS and providing novel therapeutic strategies for IBD.