文献类型：期刊文献

中文题名：壳寡糖通过促小胶质细胞M2极化缓解神经炎症

英文题名：Chitosan Oligosaccharide Alleviates Neuroinflammation by Promoting M2 Polarisation of Microglia

作者：何悦[1];蔡明扬[1];严思茹[1];孙雅煊[1];霍清[1];戴雪伶[1]

第一作者：何悦

机构：[1]北京联合大学生物化学工程学院食品与医药系,北京100023

第一机构：北京联合大学生物化学工程学院

年份：2026

卷号：26

期号：4

起止页码：50-59

中文期刊名：中国食品学报

外文期刊名：Journal of Chinese Institute of Food Science and Technology

收录：;EI(收录号：20262420926385);北大核心:【北大核心2023】；

基金：国家自然科学基金项目(11975048)。

语种：中文

中文关键词：壳寡糖;BV-2细胞;脂多糖;M2极化;STAT3

外文关键词：chitosan oligosaccharides(COS);BV-2 cells;lipopolysaccharide;M2 polarization;STAT3

摘要：目的:研究壳寡糖(COS)对脂多糖(LPS)诱导的BV-2小胶质细胞神经炎症的影响及潜在的分子机制。方法:建立LPS诱导的BV-2神经炎症模型,试验分为5组:对照组(CON组)、LPS组(100 ng/mL处理12 h)、LPS+COS低、中、高剂量组(50,100,200μg/mL的COS预处理4 h后,加入LPS处理12 h)。采用CCK-8法测定BV-2小胶质细胞活力,Griess法测定NO含量,实时荧光定量PCR分析促炎及抗炎细胞因子的mRNA表达水平。流式细胞术、Western Blot分析BV-2小胶质细胞M1表型标记物CD80、CD16、iNOS,M2表型标记物CD206和Arg-1的表达水平,以及p-STAT3/STAT3的表达情况。结果:与LPS组相比,加入COS预处理能够显著减少NO的释放。LPS处理的细胞显著上调小胶质细胞M1表型标记物(IL-1β、IL-6、TNF-α、iNOS、CD80、CD16)的表达,同时显著下调M2表型标记物(IL-4、TGF-β、CD206、Arg-1)的表达。与LPS组相比,不同质量浓度COS预处理可显著下调M1表型标记物的表达,并上调M2表型标记物的表达。此外,LPS组的p-STAT3/STAT3的蛋白表达水平显著升高,而COS可有效逆转这种趋势。结论:COS促使LPS诱导的BV-2小胶质细胞由M1表型向M2表型转变,减轻LPS诱导的神经炎症,其机制可能与抑制STAT3的激活有关。
Objective:To investigate the effect of chitosan(COS)on lipopolysaccharide(LPS)-induced neuroinflammation in BV-2 microglia and the potential molecular mechanisms.Methods:A model of LPS-induced BV-2 neuroinflammation was established,and the experiment was divided into five groups:control group(CON group),LPS group(100 ng/mL treatment for 12 h),and LPS+COS low,medium,and high-dose groups(50,100μg/mL,and 200μg/mL of COS were pretreated for 4 h,and then added to LPS treatment for 12 h).The viability of BV-2 microglia was determined by CCK-8 method,NO content by Griess method,and mRNA expression levels of pro-and anti-inflammatory cytokines were analyzed by real-time fluorescence quantitative PCR.Flow cytometry and Western Blot were used to analyze the expression levels of M1 phenotypic markers CD80,CD16,iNOS and M2 phenotypic markers CD206 and Arg-1 in BV-2 microglia,as well as the expression of p-STAT3/STAT3.Results:The addition of COS pretreatment significantly reduced NO release compared with the LPS group.The LPS-treated cells significantly up-regulated the expression of microglia M1 phenotypic markers(IL-1β,IL-6,TNF-α,iNOS,CD80,CD16),while significantly down-regulating the expression of M2 phenotypic markers(IL-4,TGF-β,CD206,Arg-1).Compared with the LPS group,pretreatment with different concentrations of COS significantly down-regulated the expression of M1 phenotypic markers and up-regulated the expression of M2 phenotypic markers.In addition,the expression level of p-STAT3/STAT3 was significantly elevated in the LPS group,while COS effectively reversed this trend.Conclusion:COS contributed to the LPS-induced shift of BV-2 microglia from M1 to M2 phenotype and attenuated LPS-induced neuroinflammation,the mechanism of which may be related to the inhibition of STAT3.