| 鲍 和,王 晨,杭建峰,王志刚,李 楠,郭 琪.黄连素通过SOCS1减轻Aβ淀粉样蛋白诱导的小胶质细胞激活[J].,2019,19(7):1222-1226 |
| 黄连素通过SOCS1减轻Aβ淀粉样蛋白诱导的小胶质细胞激活 |
| Berberine Attenuate β Amyloid-Induced Microglial Activation via SOCS1 |
| 投稿时间：2018-08-18 修订日期：2018-09-12 |
| DOI：10.13241/j.cnki.pmb.2019.07.005 |
| 中文关键词: 小胶质细胞 炎症 阿尔兹海默症 黄连素 细胞因子沉默蛋白1 |
| 英文关键词: Microglia Inflammation Alzheimer's disease Berberine SOCS1 |
| 基金项目:国家自然科学基金项目(81700644) |
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| 中文摘要: |
| 摘要 目的：观察黄连素(Berberine，BBR)对暴露于Aβ淀粉样蛋白(β Amyloid，Aβ)中的小胶质细胞激活的影响，并明确细胞因子沉默蛋白1(Silencing of Cytokine Signaling Factor 1, SOCS1)是否参与了BBR对小胶质细胞激活的影响。方法：将N9小胶质细胞暴露于含5 μM Aβ的培养基中模拟阿尔兹海默症(Alzheimer's，AD)中的小胶质细胞激活。随后，将细胞分为5组，分别为Control组、5 μM的Aβ损伤组(Aβ)、BBR+Aβ组、SOCS1-siRNA干扰组(SOCS1-siRNA+ BBR+Aβ)和乱序siRNA处理组(SC-siRNA+ BBR+Aβ)，细胞处理24 h后，采用Western blot检测细胞诱导型一氧化氮合酶(Inducible Nitric Oxide Synthase，iNOS)、SOCS1蛋白的表达，酶联免疫吸附法(Enzyme Linked Immunosorbent Assay，ELISA)检测细胞培养基内炎症因子的水平。结果：与正常培养的Control组相比，5 μM的Aβ暴露24 h可显著增加细胞iNOS蛋白表达水平和肿瘤坏死因子α(Tumor Necrosis Factor α，TNF-α)、白细胞介素1β(Interleukin 1β，IL-1β)和IL-6的释放(P<0.05)，但并未对SOCS1蛋白表达产生显著影响(P>0.05)，5 μM的BBR可显著降低iNOS表达和上述3种促炎症因子的释放(P<0.05)，并上调SOCS1蛋白表达，而SOCS1-siRNA可显著逆转BBR对iNOS和SOCS1蛋白表达及3种炎症因子释放的影响(P<0.05)。结论：BBR可能通过SOCS1减轻Aβ淀粉样蛋白对小胶质细胞的激活。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate berberine (BBR)-induced effects on microglial activation induced by β amyloid (Aβ), and explore the role of Silencing of Cytokine Signaling Factor 1(SOCS1) in BBR-induced effects on microglial activation. Methods: N9 mi- croglial cells were exposed to 5 μM Aβ to mimic microglial activation in Alzheimer's disease (AD). The microglial cells were divided into five groups, including normal cultured Control, Aβ: cells were exposed to 5 μM Aβ, BBR+Aβ: cells were exposed to 5 μM BBR plus 5 μM Aβ, SOCS1-siRNA+BBR+Aβ: cells were treated with SOCS1-siRNA and then exposed to BBR plus Aβ; SC-siRNA+BBR+Aβ: cells were treated with scrambled(SC)-siRNA and then exposed to BBR plus Aβ; after 24-h treatment, western blot and enzyme linked immunosorbent assay(ELISA) kits were taken to assess inducible nitric oxide synthase (iNOS) and SOCS1 protein expressions and pro-inflammatory cytokines in the medium. Results: Compared with the Control, 5 μM Aβ exposure increased the iNOS expression and the inflammatory cytokine secretions, including tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and IL-6 (P<0.05), but showed no significant effect on the SOCS1 expression(P>0.05), and 5 μM BBR reduced the Aβ-induced iNOS expression and the cytokine relea- ses, and increased the SOCS1 expression(P<0.05), however, SOCS1-siRNA treatment, but not the scrambled(SC)-siRNA(P>0.05), reversed the BBR-induced effects above(P<0.05). Conclusion: Our findings indicated that BBR decreased Aβ-induced microglial activa- tion via SOCS1 protein. |
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