首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Glial cell line-derived neurotrophic factor protects midbrain dopaminergic neurons against lipopolysaccharide neurotoxicity.
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Glial cell line-derived neurotrophic factor protects midbrain dopaminergic neurons against lipopolysaccharide neurotoxicity.

机译:胶质细胞系衍生的神经营养因子保护中脑多巴胺能神经元免受脂多糖神经毒性。

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摘要

Aberrant microglia activation causes dopaminergic neuronal loss and nitric oxide produced by microglia plays a critical role in dopaminergic neuronal degeneration. However, no study has determined if GDNF protects dopaminergic neurons via inhibiting nitric oxide generation in Parkinson's disease animal model. We report that GDNF not only reduces lipopolysaccharide-induced degeneration of dopaminergic neurons, suppresses microglia activation and nitric oxide generation, but also reverses the inhibition of phosphoinositide 3-kinase (PI3K) in dopaminergic neurons and microglia. It suggests that the neuroprotective effect of GDNF on dopaminergic neurons may be related to its suppression of microglia activation-mediated nitric oxide via releasing the inhibition of PI3K in both neurons and microglia.
机译:小胶质细胞的异常激活引起多巴胺能神经元的丧失,而由小胶质细胞产生的一氧化氮在多巴胺能神经元变性中起关键作用。然而,尚无研究确定GDNF是否通过抑制帕金森氏病动物模型中的一氧化氮生成来保护多巴胺能神经元。我们报道,GDNF不仅减少了脂多糖诱导的多巴胺能神经元变性,抑制了小胶质细胞的激活和一氧化氮的产生,而且还逆转了多巴胺能神经元和小胶质细胞对磷酸肌醇3激酶(PI3K)的抑制作用。这提示GDNF对多巴胺能神经元的神经保护作用可能与其通过释放神经元和小胶质细胞中PI3K的抑制作用抑制小胶质细胞激活介导的一氧化氮有关。

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