海洋环境的特殊性蕴育了多种活性显著的新颖化合物，尤其在临床缺少有效药物的难治性疾病显示独特优势，成为了新药的重要源泉。多发性硬化症(MS)是炎性介导的脱髓鞘疾病，现有药物仅可延缓疾病进程，因此，MS治疗药物的研发有着迫切的需求。本实验室前期筛选获得新型海洋真菌提取物C5可显著抑制EAE小鼠（MS动物模型）临床症状，该作用与IL10依赖型M2型巨噬细胞极化密切相关，且SOCS3和p-STAT3蛋白水平在该调控过程中明显改变。基于此，本课题将进一步明确巨噬细胞在C5治疗EAE中扮演的角色，阐明C5通过IL10/IL10R-SOCS3-STAT3信号通路调控巨噬细胞M2型极化的分子机制。通过本研究，不仅将揭示新型海洋真菌提取物C5调控巨噬细胞M2型极化在EAE治疗过程中的重要作用，还将丰富巨噬细胞M2型极化的分子机制，推动海洋来源药物在MS中的研发，最终为发现与利用结构新颖的海洋资源提供新思路。

Unique marine environment breeds a variety of novel compounds with specific activity, which shows special advantages in refractory diseases lacking effective drugs. Thus, marine lives have become an important source of new drugs. Multiple Sclerosis (MS) is the inflammatory demyelinating disease, and current therapy of MS can only delay the progression. Therefore, more effective pharmacological strategies for MS is urgently needed. We previously screened that C5, a novel marine fungus extract, could obviously ameliorate the clinical symptoms of EAE, an animal model of MS. Moreover, this effect is closely related to IL10 dependent M2 macrophage polarization, and the protein level of SOCS3 and p-STAT3 during this regulation is significantly changed. Based on these observations, this study will further identify the role of macrophages in C5-treated EAE mice, elucidate the molecular mechanism of IL10/IL10R-SOCS3-STAT3 signaling pathway in C5-mediated M2 polarization of macrophages. This research will reveal the critical role of C5-mediated macrophages M2 polarization in EAE treatment, enrich the molecular mechanism of M2-type macrophage polarization. Furthermore, it will boost the study of marine-derived drugs in MS therapy and provide the new strategies for discovering and utilizing marine-derived novel drugs.