神经损伤与功能重建2025，Vol.20Issue(2)：63-66,78,5.DOI:10.16780/j.cnki.sjssgncj.20250025
富马酸二甲酯通过激活自噬调控小胶质细胞炎症表型转化
Dimethyl Fumarate Regulates the Inflammatory Phenotype Transformation of Microglia via Activating Autophagy
摘要
Abstract
Objective:To explore in vitro the effect and mechanism of dimethyl fumarate(DMF)on modulat-ing microglial polarization under chronic hypoperfusion-induced white matter injury(WMI).Methods:An in vitro model of low perfusion white matter demyelination was established by glucose-oxygen deprivation and stimulation with exogenous myelin debris,combined with DMF intervention in microglial cells.Real-time quan-titative PCR,transcriptome sequencing,and immunofluorescence staining were employed to investigate the in-flammatory phenotype transformation of microglia.Results:(1)Compared to the control group,the expression of pro-inflammatory genes interleukin(IL)-6,IL-1β and tumor necrosis factor(TNF)-α significantly decreased after DMF administration(P＜0.05);(2)Transcriptome analysis revealed downregulation of neuroinflamma-tion-related pathways and upregulation of autophagy-related pathways in microglia after DMF treatment;(3)Compared to the control group,the expression of autophagy-related genes and proteins was significantly in-creased in the DMF intervention group(P＜0.05).Conclusion:DMF may regulate the transformation of microg-lia from a pro-inflammatory to an anti-inflammatory phenotype by activating the autophagy pathway.关键词
小胶质细胞/富马酸二甲酯/自噬/炎症表型Key words
microglia cells/dimethyl fumarate/autophagy/inflammatory phenotype分类
临床医学引用本文复制引用
诸丽芳,张航,庞晓伟,初云惠,张璐阳,秦川,田代实..富马酸二甲酯通过激活自噬调控小胶质细胞炎症表型转化[J].神经损伤与功能重建,2025,20(2):63-66,78,5.基金项目
国家自然科学基金项目(自噬介导小胶质细胞代谢重编程参与慢性低灌注脑白质损伤的机制研究,No.82071380) （自噬介导小胶质细胞代谢重编程参与慢性低灌注脑白质损伤的机制研究,No.82071380）
