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(P〈0.05),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(P〈0.05),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。
Objective: To investigate the effect of curcumin (Cur) on lipopolysaccharide (LPS)-induced microglial actwatlon and the 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 model of microglial inflammation. ELISA was used to assess the concentrations of tumor necrosis factor ct (TNF-a), interleukin (IL)-1β and IL-6. Phase contrast microscope was used to record the morphology of microglial cells exposed to LPS. Immunocytochemistry and western blot were used to measure the expression of TOLR4. Results: Compared with that in the control, LPS of 100 ng/ml increased the concentrations of TNF-α, IL-1β and IL-6 in the supematant (P〈0.05), while curcumin of 10 μM decreased the levels of TNF-α, IL-1β and IL-6 markedly (P〈0.05). In addition, curcumin ameliorated the morphology and decreased the expression of TOLR4 in microglial cells exposed to LPS. Conclusion: Curcumin attenuated microglial activation induced by LPS, and the inhibition of TOLR4 may be associated with the effect.