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姜黄素对小胶质细胞的活化的影响
引用本文:靳晓芳 郭琪 李蓓 马宝玉 王晨. 姜黄素对小胶质细胞的活化的影响[J]. 现代生物医学进展, 2014, 14(32): 6257-6259
作者姓名:靳晓芳 郭琪 李蓓 马宝玉 王晨
作者单位:西安市第四医院药剂科
基金项目:国家自然科学基金项目(81171237)
摘    要:目的:研究姜黄素对脂多糖引起的小胶质细胞活化状态的影响,并探讨TOLR4受体在其中的作用。方法:采用体外培养N9小鼠小胶质细胞系,脂多糖作为刺激,激活小胶质细胞。采用ELISA法检测小胶质细胞培养基中TNF-α、IL-1β和IL-6的含量;相差显微镜观测细胞形态;免疫细胞化学和western blot观测小胶质细胞TOLR4受体表达情况。结果:与对照组相比,暴露于100ng/ml脂多糖24 h的小胶质细胞促炎症因子TNF-α、IL1β和IL-6释放量明显增加(P0.05),姜黄素浓度为10μM时,可显著减少小胶质细胞释放TNF-α、IL-1β和IL-6(P0.05),此外,姜黄素还可改善小胶质细胞形态,并降低暴露于脂多糖中的小胶质细胞TOLR4受体的表达。结论:姜黄素可能通过抑制TOLR4表达,减轻了脂多糖对小胶质细胞的激活。

关 键 词:小胶质细胞  姜黄素  炎症  TOLR4  脂多糖

The Effect of Curcumin on Microglial Activation
JIN Xiao-fang,GUO Qi,LI Bei,MA Bao-yu,WANG Chen. The Effect of Curcumin on Microglial Activation[J]. Progress in Modern Biomedicine, 2014, 14(32): 6257-6259
Authors:JIN Xiao-fang  GUO Qi  LI Bei  MA Bao-yu  WANG Chen
Affiliation:JIN Xiao-fang;GUO Qi;LI Bei;MA Bao-yu;WANG Chen;Department of Pharmacology, Xi’an No.4 Hospital;
Abstract:Objective:To investigate the effect of curcumin (Cur) on lipopolysaccharide (LPS)-induced microglial activation andthe role of Toller Receptor 4 (TOLR4) in the effect.Methods:N9 microglia cell line exposed to LPS for 24 h was used to mimic the modelof microglial inflammation. ELISA was used to assess the concentrations of tumor necrosis factor alpha(TNF-alpha), interleukin (IL)-1beta andIL-6. Phase contrast microscope was used to record the morphology of microglial cells exposed to LPS. Immunocytochemistry and westernblot were used to measure the expression of TOLR4.Results:Compared with that in the control, LPS of 100 ng/ml increased the concentrationsof TNF-alpha, IL-1beta and IL-6 in the supernatant (P<0.05), while curcumin of 10 uM decreased the levels of TNF-alpha, IL-1beta andIL-6 markedly (P<0.05). In addition, curcumin ameliorated the morphology and decreased the expression of TOLR4 in mi- croglial cellsexposed to LPS.Conclusion:Curcumin attenuated microglial activation induced by LPS, and the inhibition of TOLR4 may be associatedwith the effect.
Keywords:Microglia   Curcumin   Inflammation   TOLR4   Lipopolysaccharide
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