Li Feng-Qiao, Lu Xiu-Zhi, Liang Xi-Bin, Zhou Hui-Fang, Xue Bing, Liu Xian-Yu, Niu Dong-Bin, Han Ji-Sheng, Wang Xiao-Min
Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100083, PR China.
J Neuroimmunol. 2004 Mar;148(1-2):24-31. doi: 10.1016/j.jneuroim.2003.10.054.
Mounting lines of evidence have suggested that brain inflammation participates in the pathogenesis of Parkinson's disease. Triptolide is one of the major active components of Chinese herb Tripterygium wilfordii Hook F, which possesses potent anti-inflammatory and immunosuppressive properties. We found that triptolide concentration-dependently attenuated the lipopolysaccharide (LPS)-induced decrease in [3H]dopamine uptake and loss of tyrosine hydroxylase-immunoreactive neurons in primary mesencephalic neuron/glia mixed culture. Triptolide also blocked LPS-induced activation of microglia and excessive production of TNFalpha and NO. Our data suggests that triptolide may protect dopaminergic neurons from LPS-induced injury and its efficiency in inhibiting microglia activation may underlie the mechanism.
越来越多的证据表明，脑部炎症参与帕金森病的发病机制。雷公藤甲素是中药雷公藤的主要活性成分之一，具有强大的抗炎和免疫抑制特性。我们发现，在原代中脑神经元/胶质细胞混合培养中，雷公藤甲素浓度依赖性地减弱脂多糖（LPS）诱导的[3H]多巴胺摄取减少和酪氨酸羟化酶免疫反应性神经元的丢失。雷公藤甲素还阻断LPS诱导的小胶质细胞活化以及TNFα和NO的过量产生。我们的数据表明，雷公藤甲素可能保护多巴胺能神经元免受LPS诱导的损伤，其抑制小胶质细胞活化的功效可能是其作用机制的基础。
