肠神经系统(ENS)损伤目前尚缺乏有效治疗手段。本课题立足于“骨髓基质干细胞（MSCs）可通过激活肠神经前体细胞（ENPC）促进ENS重建，但再生神经元功能尚不成熟”这一原创性成果，首次提出岩藻糖基化修饰可从4个维度优化ENS重建过程：优化MSCs的定向迁移；优化MSCs的类胶质细胞的活性；优化肠神经前体细胞（ENPC）的激活；优化再生神经元成熟。并以在MSCs类胶质细胞特性、ENPC活化及再生神经元成熟中均发挥重要作用的PI3K/AKT/mTOR信号通路为切入点，探讨该通路中关键蛋白的岩藻糖基化修饰对优化ENS重建过程的作用，挖掘糖基化修饰和磷酸化修饰相互作用的机制和意义。糖基化修饰作为一种特殊的蛋白质修饰方式，手段温和，具有独特的优越性。结合消化内镜应用的普适性，深入研究岩藻糖基化修饰在促进“MSCs介导的ENS修复”中的作用和机制，将可能为胃肠道动力障碍性疾病的临床治疗提供新的视野。

Enteric nervous system (ENS) injury currently lacks effective treatment. Based on the research that “Bone marrow stromal cells (MSCs) promote ENS reconstitution, but the regenerative neuronal function still need to be improved”, we proposed that fucosylation modification can play an important role in optimizing MSCs-ENS nerve repair process by promoting directional migration of MSCs, stimulating GDNF secretion, promoting ENPC differentiation to neurons, and promoting regenerative neuron maturation in multiple dimensions. We also used the PI3K/AKT/mTOR signaling pathway, which plays an important role in the maturation of MSCs (GDNF secretion), ENPC activation, and regenerative neuron maturation, to explore the role of key protein glycosylation and phosphorylation interactions in the PI3K/AKT/mTOR pathway in optimizing MSCs-mediated ENS reconstitution. As a special modification method, fucosylation modification is mild and has unique advantages. Combined with the universality of digestive endoscopy, in-depth study of fucosylation modification to optimize the role and mechanism of "MSCs-mediated ENS repair" will provide a new perspective for the clinical treatment of gastrointestinal motility disorders.