Sirt1/PGC1α通路的激活可减轻帕金森病的神经炎症损伤

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yang Yang, Zhongying Gong, Zhiyun Wang, Yi Lu
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引用次数: 2

摘要

帕金森氏症是一种脑部疾病,其特征是震颤性麻痹,会影响运动系统。帕金森病的发病机制被认为是神经退行性疾病、神经氧化应激、神经炎症和神经递质紊乱。在本研究中,我们探讨了Sirt1/PGC1α通路在TNFα作用下对BV-2细胞活力的调节作用。我们的研究结果表明,Sirt1/PGC1α通路的活性在TNFα处理下显着下调。在体外神经炎症模型下,通过补充SRT1720重新激活Sirt1/PGC1α通路可显著提高BV-2细胞的活力。因此,我们的研究结果报告了一种新的信号通路,负责神经炎症下神经元的存活。Sirt1/PGC1α通路的再激活可能是通过增强神经元活力来治疗帕金森病的潜在治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Activation of Sirt1/PGC1α pathway attenuates neuroinflammation injury in Parkinson's disease.

Parkinson's disease is a brain disorder that is featured by shaking palsy, which affect the motor system. The pathogenesis of Parkinson's disease has been ascribed to neurodegenerative disorder, neural oxidative stress, neuroinflammation, and neurotransmitter disorder. In the present study, we explored the influence of Sirt1/PGC1α pathway in regulating BV-2 cells viability under TNFα treatment. Our results demonstrated that the activity of Sirt1/PGC1α pathway was significantly downregulated in response to TNFα treatment. Reactivation of Sirt1/PGC1α pathway through supplementation of SRT1720 significantly elevated the viability of BV-2 cells under an in vitro neuroinflammation model. Therefore, our results report a novel signaling pathway responsible for the survival of neuron under neuroinflammation. Re-activation of Sirt1/PGC1α pathway may be a potential therapeutic approach for the treatment of Parkinson's disease through enhancing neuronal viability.

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来源期刊
Journal of Receptors and Signal Transduction
Journal of Receptors and Signal Transduction 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.
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