Abstract

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.

摘要

帕金森病是一种脑部疾病，其特征是颤抖性麻痹，影响运动系统。帕金森病的发病机制已归因于神经退行性疾病、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 处理下调节 BV-2 细胞活力的影响。我们的结果表明，响应于 TNFα 处理，Sirt1/PGC1α 通路的活性显着下调。通过补充 SRT1720 重新激活 Sirt1/PGC1α 通路显着提高了体外体外BV-2 细胞的活力神经炎症模型。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通路的重新激活可能是一种通过增强神经元活力来治疗帕金森病的潜在治疗方法。