文献类型：期刊文献

英文题名：Chitooligosaccharide ameliorates cognitive deficits and neuroinflammation in APP/PS1 mice associated with the regulation of Nrf2/NF-κB axis

作者：Cai, Mingyang[1,2];Zhang, Xiaoxia[1];Gao, Xiaohan[1];Huo, Qing[2];Sun, Yaxuan[1,2];Dai, Xueling[1,2]

第一作者：Cai, Mingyang

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;[2]Beijing Union Univ, Coll Biochem Engn, Dept Food Sci & Biomed, 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

卷号：303

外文期刊名：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

收录：;EI(收录号：20250617818370);Scopus(收录号：2-s2.0-85216846939);WOS:【SCI-EXPANDED(收录号:WOS:001423300900001)】；

基金：This research was supported by grants from the Beijing Natural Science Foundation (6164030) , National Natural Science Foundation of China (11975048) , 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：Chitooligosaccharide; Cognitive deficits; Neuroinflammation; Nrf2; NF-kappa B; NLRP3 inflammasome

摘要：Mounting evidence suggests that neuroinflammation is involved in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD). Amyloid (3 peptide (A(3) could recruit and activate microglia, leading to the generation of pro-inflammatory factors, and ultimately neuroinflammation. Chitooligosaccharide (COS) is widely recognized as anti-inflammation bioactive substance, though whether it exerts beneficial effect on AD is unclear. In this study, we explored the effect of COS on AD prevention and treatment. We found that COS ameliorated cognitive deficiency, increased the expression of Nrf2 but decreased A(3 levels and the activation of NF-kappa B in APP/PS1 mice. In vitro, COS decreased the secretions of IL-6, IL-1(3 and TNF-alpha in A(325-35 + lipopolysaccharides (LPS)-exposed BV2 microglia. Meanwhile, COS down-regulated the expressions of iNOS, COX-2, NLRP3, caspase 1 and the nuclear translocation of NF-kappa B p65, while upregulated the expressions of Nrf2 and HO-1. Further, COS improved the viability of SK-N-SH cells that exposed to A(325-35 + LPS-stimulated microglial conditioned media, and the repressive effect of COS on NLRP3, iNOS, and phospho-NF-kappa B p65 expressions were markedly compromised upon Nrf2-siRNA transfection. Collectively, COS improved cognitive decline and suppressed neuroinflammation via the Nrf2/NF-kappa B signaling axis, suggesting COS might be a promising candidate in down-regulating inflammatory responses during AD progression.