Zhou Hui-Fang, Niu Dong-Bin, Xue Bing, Li Feng-Qiao, Liu Xian-Yu, He Qi-Hua, Wang Xin-Hong, Wang Xiao-Min
Neuroscience Research Institute, Peking University, Beijing, PR China.
Neuroreport. 2003 May 23;14(7):1091-5. doi: 10.1097/01.wnr.0000073682.00308.47.
Microglia are believed to participate in the mediation of neurodegeneration through producing a variety of cytotoxic factors upon activation. Pharmacological intervention in microglial activation may therefore exert a neuroprotective effect. In exploring pharmacological agents that can affect microglial activation, we found in this study that triptolide possesses a powerful inhibitory influence over microglia. Pretreatment with triptolide was able to dose-dependently reduce the lipopolysaccharide (LPS)-induced nitrite accumulation and tumor necrosis factor-alpha and interleukin-1beta release from LPS-activated microglia as revealed by Griess reaction and ELISA, respectively. Triptolide reduced LPS-stimulated mRNA expression of all three inflammatory factors. The results obtained from this study demonstrate that triptolide can inhibit inflammatory responses of microglia to inflammatory stimulation via a mechanism involving the inhibition of the synthesis and release of inflammatory factors.
小胶质细胞被认为通过激活后产生多种细胞毒性因子参与神经退行性变的介导。因此，对小胶质细胞激活的药理学干预可能发挥神经保护作用。在探索能够影响小胶质细胞激活的药物制剂时，我们在本研究中发现雷公藤内酯醇对小胶质细胞具有强大的抑制作用。如分别通过格里斯反应和酶联免疫吸附测定法所显示的，用雷公藤内酯醇预处理能够剂量依赖性地减少脂多糖（LPS）诱导的亚硝酸盐积累以及LPS激活的小胶质细胞中肿瘤坏死因子-α和白细胞介素-1β的释放。雷公藤内酯醇降低了所有三种炎症因子的LPS刺激的mRNA表达。本研究获得的结果表明，雷公藤内酯醇可通过涉及抑制炎症因子合成和释放的机制抑制小胶质细胞对炎症刺激的炎症反应。
