Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Korea.
Neurobiol Aging. 2012 Sep;33(9):2145-59. doi: 10.1016/j.neurobiolaging.2011.08.011. Epub 2011 Oct 27.
Amantadine is currently used as an antiviral and an antiparkinsonian drug. Although the drug is known to bind a viral proton channel protein, the mechanism of action in Parkinson's disease (PD) remains to be determined. This study investigated whether the drug has an inhibitory effect on microglial activation and neuroinflammation, which have been implicated in the progression of neurodegenerative processes. Using cultured microglial cells, it was demonstrated that the drug inhibited inflammatory activation of microglia and a signaling pathway that governs the microglial activation. The drug reduced the expression and production of proinflammatory mediators in bacterial lipopolysaccharide-stimulated microglia cells. The microglia-inhibiting activity of amantadine was also demonstrated in a microglia/neuron coculture and animal models of neuroinflammation and Parkinson's disease. Collectively, our results suggest that amantadine may act on microglia in the central nervous system to inhibit their inflammatory activation, thereby attenuating neuroinflammation. These results provide a molecular basis of the glia-targeted mechanism of action for amantadine.
金刚烷胺目前被用作抗病毒和抗帕金森病药物。尽管该药物已知可结合病毒质子通道蛋白,但在帕金森病(PD)中的作用机制仍有待确定。本研究调查了该药物是否对小胶质细胞激活和神经炎症具有抑制作用,因为这些因素与神经退行性过程的进展有关。使用培养的小胶质细胞表明,该药物抑制了小胶质细胞的炎症激活和控制小胶质细胞激活的信号通路。该药物减少了细菌脂多糖刺激的小胶质细胞中促炎介质的表达和产生。金刚烷胺在小胶质细胞/神经元共培养物以及神经炎症和帕金森病动物模型中也表现出抑制小胶质细胞的活性。总的来说,我们的结果表明,金刚烷胺可能作用于中枢神经系统中的小胶质细胞以抑制其炎症激活,从而减轻神经炎症。这些结果为金刚烷胺的靶向神经胶质作用机制提供了分子基础。