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阿魏酸苯乙酯预防 1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的神经退行性变。

Caffeic acid phenethyl ester prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration.

机构信息

Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

出版信息

Neuroscience. 2011 Aug 11;188:135-41. doi: 10.1016/j.neuroscience.2011.04.009. Epub 2011 May 6.

Abstract

Parkinson's disease is associated with the loss of dopaminergic neurons in the substantia nigra and decreased striatal dopamine levels. We now report that caffeic acid phenethyl ester (CAPE), an active component of propolis, attenuated dopaminergic neurodegeneration and dopamine loss in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson's disease. The neuroprotective effect of CAPE was associated with marked reductions in inducible nitric oxide synthase (iNOS) and caspase 1 expression. Additionally, CAPE inhibited MPP+-induced neurotoxicity in vitro and directly inhibited MPP+-induced release of cytochrome c and apoptosis inducing factor (AIF) from mitochondria. Thus, CAPE may have beneficial effects in slowing or preventing the progression of Parkinson's disease and other neurodegenerative disorders.

摘要

帕金森病与黑质中多巴胺能神经元的丧失和纹状体多巴胺水平降低有关。我们现在报告,咖啡酸苯乙酯(CAPE),一种蜂胶的活性成分,可减轻帕金森病 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)小鼠模型中的多巴胺能神经退行性变和多巴胺丢失。CAPE 的神经保护作用与诱导型一氧化氮合酶(iNOS)和半胱天冬酶 1 表达的显著减少有关。此外,CAPE 抑制了 MPP+诱导的体外神经毒性,并直接抑制了 MPP+诱导的细胞色素 c 和凋亡诱导因子(AIF)从线粒体释放。因此,CAPE 可能对减缓或预防帕金森病和其他神经退行性疾病的进展有有益的影响。

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