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首页> 外文期刊>The European Journal of Neuroscience >Broad neuroprotective profile of nicotinamide in different mouse models of MPTP-induced parkinsonism.
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Broad neuroprotective profile of nicotinamide in different mouse models of MPTP-induced parkinsonism.

机译：烟酰胺在MPTP诱发的帕金森病不同小鼠模型中具有广泛的神经保护作用。

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The factors contributing to substantia nigra pars compacta (SNc) dopamine (DA) neuron death and striatal DA depletion in Parkinson's disease (PD) are still poorly understood. However, mitochondrial dysfunction, cellular energy depletion and oxidative stress appear to play important roles in the pathogenesis of PD. In view of this, the current study examined the potential of nicotinamide, a form of the B-complex vitamin niacin, to protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced SNc cell loss and striatal DA depletion in two mouse MPTP models that respond differently to putative neuroprotective agents. Adult male C57Bl/6 mice received nicotinamide (125, 250 or 500 mg/kg i.p.) prior to either acute (four injections in 1 day at 2-h intervals) or sub-acute (two injections per day at 4-h intervals for 5 days) MPTP administration. Striatal DA levels, changes in numbers of tyrosine hydroxylase (TH)- and cresyl violet-stained cells in the SNc at 2 and 6 weeks following the last MPTP exposure were analyzed. Nicotinamide administration resulted in a dose-dependent sparing of striatal DA levels and SNc neurons in acute MPTP-treated animals. Only the highest dose of nicotinamide had similar effects in sub-acute MPTP-treated animals. At 6 weeks after MPTP exposure, there was some spontaneous recovery of striatal DA levels in both models: neuroprotective effects were still apparent in acute but not sub-acute MPTP-treated animals. These results show neuroprotective effects of nicotinamide in different mouse Parkinson models associated with different forms of cell death and suggest that nicotinamide may have broad neuroprotective potential in PD.
机译：帕金森病（PD）中促成黑质致密部（SNc）多巴胺（DA）神经元死亡和纹状体DA消耗的因素仍然知之甚少。然而，线粒体功能障碍，细胞能量消耗和氧化应激似乎在PD的发病机理中发挥重要作用。有鉴于此，当前的研究研究了烟酰胺（一种B族复合维生素烟酸）对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的SNc的保护作用的潜力。两种对假定的神经保护剂反应不同的小鼠MPTP模型中的细胞损失和纹状体DA耗竭。成年雄性C57Bl / 6小鼠在急性（每2h间隔1天注射4次）或亚急性（每天2h间隔4h注射两次）之前接受烟酰胺（125、250或500 mg / kg ip）。 5天）MPTP管理。分析了最后一次MPTP暴露后2周和6周，SNc中的纹状体DA水平，酪氨酸羟化酶（TH）和甲酚紫染色细胞数量的变化。在急性MPTP处理的动物中，烟酰胺的给药导致纹状体DA水平和SNc神经元的剂量依赖性降低。在MPTP亚急性治疗的动物中，仅最高剂量的烟酰胺具有相似的作用。在MPTP暴露后第6周，两种模型中的纹状体DA水平都有自发恢复：在急性但经MPTP处理的非急性动物中神经保护作用仍然明显。这些结果表明烟酰胺在与不同形式的细胞死亡相关的不同小鼠帕金森病模型中的神经保护作用，并表明烟酰胺在PD中可能具有广泛的神经保护潜力。

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