| 乌帕替尼对氧糖剥夺/复氧后BV2细胞极化的影响 |
| 投稿时间：2020-12-03 修订日期：2021-02-26 点此下载全文 |
| 引用本文：宋志兵,张倩,章越凡,邱彦,李铁军.乌帕替尼对氧糖剥夺/复氧后BV2细胞极化的影响[J].药学实践杂志,2021,39(2):112~117 |
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| 基金项目:浦东新区卫生系统学科建设项目（新兴、交叉学科-精准临床药学，PWXx2020-03）；浦东新区卫生和计划生育委员会学科建设项目（重要薄弱学科-临床药学，PWZbr2017-16）；上海市健康医学院协同创新重大专项（SPCI-18-13-001） |
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| 中文摘要:目的 研究乌帕替尼对氧糖剥夺再复氧（OGD/R）后BV2小胶质细胞极化及炎症的影响，并探讨其作用机制。方法 实验分对照组、OGD组和乌帕替尼组3组。BV2细胞经OGD/R处理后，噻唑蓝试剂(MTT)检测细胞生存率，划痕实验观察细胞迁移能力，实时荧光定量多聚核苷酸链式反应(qPCR)检测BV2细胞M1型极化标志物（CD11b、CD32、iNOS）和M2型极化标志物（Arg-1、IL-10、CD206）的mRNA水平，酶联免疫吸附测定(ELISA)检测培养基中IL-1β、IL-6、TNF-α含量，蛋白质印迹法(Western Blot)检测JAK1/STAT6通路相关蛋白表达水平。结果 乌帕替尼能增加OGD/R后BV2细胞的生存率（P<0.05），能减少BV2细胞向M1型极化（P<0.05）。乌帕替尼可明显降低OGD/R诱导的BV2细胞的迁移能力（P<0.05），减少OGD/R诱导BV2细胞分泌的炎症因子：IL-1β、IL-6、TNF-α（P<0.05）。乌帕替尼提高共培养PC12细胞的生存率（P<0.05）。乌帕替尼可显著抑制由OGD/R诱导激活BV2细胞p-JAK1和p-STAT6蛋白的表达水平（P<0.05）。结论 乌帕替尼可减少OGD/R诱导BV2细胞向M1型极化和减少炎症反应，与JAK1/STAT6通路有关。 |
| 中文关键词:乌帕替尼 氧剥夺/复氧 极化，炎症，酪氨酸激酶/信号传导及转录激活因子 |
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| Effects of upadacitinib on BV2 cells after oxygen–glucose deprivation/recovery |
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| Abstract:Objective To investigate the effects of upadacitinib on the polarization and inflammation of BV2 microglia after oxygen glucose deprivation/recovery (OGD/R) and to explore its mechanism of action.Methods The experiment was divided into 3 groups: control group, OGD group and upadacitinib treatment group. After BV2 cells were treated with OGD/R, MTT was used to detect cell survival rate. Wound scratch assay was used to detect the cell migration ability. qPCR was used to detect mRNA levels of M1-type polarization markers (CD11b, CD32, iNOS) and M2-type polarization markers (Arg-1, IL-10, CD206) of BV2 cells. ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in the culture medium. Western blot was used to detect the expression levels of JAK1/STAT6 pathway-related proteins.Results Upadacitinib increased the survival of BV2 cells after OGD/R (P<0.05), reduced the polarization of BV2 cells to M1 type (P<0.05). Upadacitinib significantly decreased the migration ability of BV2 cells induced by OGD/R (P<0.05), reduced the inflammatory factors secreted by BV2 cells induced by OGD/R: IL-1β, IL-6, TNF-α (P<0.05). Upadacitinib increased the survival rate of co-cultured PC12 cells (P<0.05). Upadacitinib significantly inhibited the expression levels of p-JAK1 and p-STAT6 proteins in BV2 cells activated by OGD/R induction (P<0.05).Conclusion Upadacitinib decreases polarization of BV2 induced by OGD/R to M1 type and reduces inflammation, which is related to JAK1/STAT6 pathway. |
| keywords:upadacitinib OGD/R polarization, inflammation, JAK/STAT |
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