中国免疫学杂志2024，Vol.40Issue(9)：1833-1837,5.DOI:10.3969/j.issn.1000-484X.2024.09.007
法舒地尔通过抑制NLRP3炎症小体激活抑制Aβ1-42诱导的小胶质细胞炎症反应
Fasudil inhibits Aβ1-42-induced microglial inflammatory response by inhibiting activation of NLRP3 inflammasome
摘要
Abstract
Objective:To explore mechanism of Fasudil reducing Aβ1-42 induced BV2 cell injury based on NLRP3 inflamma-some.Methods:BV2 cells were divided into:normal control group,Aβ stimulation group,Aβ+Fasudil intervention group,Aβ+MCC950(NLRP3 inhibitor)intervention group.Cell morphology was observed under microscope.Cell activity was determined of by CCK8.NO release was measured by Griess.NLRP3,caspase 1 and IL-18 expressions were detected by immunofluorescence staining.NLRP3,ASC,caspase 1,IL-1β and IL-18 expressions were detected by Western blot.Results:Compared with normal control group,BV2 cells in Aβ stimulation group were activated and showed amoeba-like shape,cell activity was decreased,NO production was increased,NLRP3,ASC,caspase 1,IL-1β and IL-18 expressions were increased.Fasudil intervention and MCC950 intervention inhibited cell injury induced by Aβ1-42 in which BV2 cell morphology tended to be normal,cell activity was increased,while produc-tion of NO was reduced,and NLRP3,ASC,caspase 1,IL-1β and IL-18 expressions were down-regulated,there was no significant difference between Fasudil intervention group and MCC950 intervention group.Conclusion:Fasudil may alleviate Aβ1-42 induced BV2 cell injury and inflammatory reaction by inhibiting NLRP3 inflammasome activation.关键词
法舒地尔/小胶质细胞/NLRP3炎症小体/炎症反应Key words
Fasudil/Microglia/NLRP3 inflammasome/Inflammatory reaction分类
医药卫生引用本文复制引用
郭敏芳,尉杰忠,马存根,章培军,于婧文,孟涛,李艳花,李娜,李梦迪,李玉璐,宋丽娟..法舒地尔通过抑制NLRP3炎症小体激活抑制Aβ1-42诱导的小胶质细胞炎症反应[J].中国免疫学杂志,2024,40(9):1833-1837,5.基金项目
山西省基础研究计划项目(20210302123476,20210302123475,20210302123337) （20210302123476,20210302123475,20210302123337）
山西省卫生健康委医学科技领军团队项目(2020TD05) （2020TD05）
国家中医药管理局多发性硬化益气活血重点研究室开放项目(2021-KF-04T) （2021-KF-04T）
山西中医药大学青年科学家培育项目(2021-PY-QN-09) （2021-PY-QN-09）
山西中医药大学2022年度科技创新团队项目(2022TD2010). （2022TD2010）
