Article Summary
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].现代生物医学进展英文版,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
Received:August 18, 2018  Revised:September 12, 2018
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)
Author NameAffiliationE-mail
BAO He Department of Pharmacology, the Second Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, China baohexjtu@163.com 
WANG Chen Department of Pharmacy, The Second Affiliated Hospital of Air Force Medical University, Xi'an, Shaanxi, 710003, China  
HANG Jian-feng Department of Laboratory, Guangzhou General Hospital of the PLA, Guangzhou, Guangdong, 510010, China  
WANG Zhi-gang Department of Nephrology, the First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China  
LI Nan Department of Pharmacology, the Second Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, China  
GUO Qi Department of Pharmacology, the Affiliated Guangren Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, 710003, China  
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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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