基于肠道菌群研究浒苔硫酸多糖ECP的抗炎症性肠病作用及其药理学机制

炎症性肠病（IBD）是一种复杂的慢性肠道炎症疾病。研究表明，肠道菌群紊乱是IBD的重要诱发因素，因此，通过靶向调节肠道菌群紊乱开发新型抗IBD药物具有重要意义。本实验室前期研究发现，条浒苔来源的硫酸多糖（ECP）可显著改变小鼠肠道菌群结构，增加肠道乳酸杆菌、双歧杆菌和阿克曼氏菌等益生菌的含量。然而，其能否通过改善肠道菌群紊乱发挥抗IBD作用尚未得到研究。本课题拟从肠道菌群角度出发，围绕这一新型药物作用靶点，以葡聚糖硫酸钠（DSS）诱导的IBD小鼠为模型，结合基因组学、生物信息学和代谢组学技术，尤其是粪菌移植及厌氧微生物体外模拟发酵技术，系统研究ECP的抗IBD作用并阐明其药理学机制，为抗IBD新药的研发奠定理论基础。

Inflammatory bowel disease (IBD) is a complex and chronic inflammatory disease in the large intestine. Accumulating evidence indicates that gut dysbiosis is a major contributor to the development of IBD. In this regard, it is critically important to develop new anti-IBD drugs by targeting the gut microbiota and attenuating dysbiosis. Our previous work in the lab illustrates that a sulfated polysaccharide from Enteromorpha clathrate (ECP) could significantly change the structure of the gut microbiota and increase the abundance of Lactobacillus spp., Bifidobacterium spp. and Akkermansia muciniphila in mice. However, whether or not ECP could help to alleviate IBD by attenuating gut dysbiosis has not been studied. In this project, starting from the perspective of gut microbiota, a new drug target, and applying a dextran sulfate sodium (DSS)-induced mouse model of IBD, we will systematically investigate the therapeutic effect of ECP on IBD and demonstrate its pharmacological mechanisms by combining a serious of techniques including genomics, bioinformatics, metabolomics, and especially fecal microbiota transplantation and in vitro simulated anaerobic fermentation. We hope that our project will lay a foundation for the development of new anti-IBD drugs.