Chen Han-Qing, Jin Zheng-Yu, Li Guan-Hong
School of Food Science and Technology, Southern Yangtze University, 1800 Lihu Road, Wuxi, Jiangsu 214122, P.R. China.
Neurosci Lett. 2007 May 1;417(2):112-7. doi: 10.1016/j.neulet.2006.11.045. Epub 2007 Mar 30.
Activation of microglia and consequent release of proinflammatory factors, are believed to contribute to neurodegeneration in Parkinson's disease (PD). Hence, identification of compounds that prevent microglial activation is highly desirable in the search for therapeutic agents for inflammation-mediated neurodegenerative diseases. In this study, we reported that biochanin A, one of the predominant isoflavones in Trifolium pratense, attenuated lipopolysaccharide (LPS)-induced decrease in dopamine uptake and the number of dopaminergic neurons in a dose-dependent manner in rat mesencephalic neuron-glia cultures. Moreover, biochanin A also significantly inhibited LPS-induced activation of microglia and production of tumor necrosis factor-alpha, nitric oxide and superoxide in mesencephalic neuron-glia cultures and microglia-enriched cultures. This study suggested for the first time that biochanin A protected dopaminergic neurons against LPS-induced damage through inhibition of microglia activation and proinflammatory factors generation.
小胶质细胞的激活以及随之而来的促炎因子释放，被认为与帕金森病（PD）中的神经退行性变有关。因此，在寻找炎症介导的神经退行性疾病治疗药物时，鉴定能够阻止小胶质细胞激活的化合物是非常必要的。在本研究中，我们报告了红车轴草中主要的异黄酮之一染料木黄酮，在大鼠中脑神经元-胶质细胞培养物中，以剂量依赖的方式减轻了脂多糖（LPS）诱导的多巴胺摄取减少和多巴胺能神经元数量减少。此外，染料木黄酮还显著抑制了LPS诱导的中脑神经元-胶质细胞培养物和富含小胶质细胞的培养物中小胶质细胞的激活以及肿瘤坏死因子-α、一氧化氮和超氧化物的产生。本研究首次表明，染料木黄酮通过抑制小胶质细胞激活和促炎因子生成，保护多巴胺能神经元免受LPS诱导的损伤。
