文献类型：期刊文献

英文题名：Chitosan Oligosaccharide Attenuates Neuroinflammation by Regulating Microglial Immunometabolic Reprogramming via the mTOR Signaling Pathway

作者：Chen, Hongli[1];Cai, Mingyang[1];He, Yue[1];Sun, Yaxuan[1];Dai, Xueling[1]

第一作者：Chen, Hongli

通讯作者：Dai, XL[1]

机构：[1]Beijing Union Univ, Coll Biochem Engn, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100023, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Coll Biochem Engn, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100023, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份：2025

外文期刊名：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001570820500001)】；

基金：This research was supported by grants from the Beijing Natural Science Foundation (6164030), Beijing Key Laboratory of Bioactive Substances and Functional Foods Research Project, the Academic Research Projects of Beijing Union University (ZK80202102), and Education Reform Project of Beijing Union University (JY2023Y008).

语种：英文

外文关键词：microglia; chitosan oligosaccharide (COS); neuroinflammation; immunometabolic reprogramming; M2 polarization; oxidative phosphorylation (OXPHOS); mTOR signaling pathway

摘要：Microglia, the primary immune cells in the central nervous system (CNS), undergo immunometabolic reprogramming under neuroinflammatory conditions. Chitosan oligosaccharide (COS) exhibits multiple biological activities, including anti-inflammatory and antioxidant effects, yet its influence on microglial metabolism remains unclear. Here, we demonstrate that lipopolysaccharide (LPS) triggers immunometabolic alterations in microglia via the mechanistic target of the rapamycin (mTOR) pathway. COS effectively normalized immunometabolism by modulating mTOR signaling, enhancing oxidative phosphorylation (OXPHOS), attenuating anaerobic glycolysis and pentose phosphate pathway (PPP) activation, promoting M2 polarization, and increasing adenosine triphosphate (ATP) production. In vivo, COS suppressed mTOR activation in the hippocampal and cortical regions, improved cognitive and spatial memory, and reduced neuronal damage in LPS-challenged mice. These findings suggest that COS modulates microglial immunometabolic reprogramming through mTOR signaling, thereby augmenting immune homeostasis and cognitive performance. In conclusion, our findings propose COS as a promising therapeutic candidate for the prevention and treatment of neuroinflammation-related disorders.