帕金森病中的异槲皮素神经保护分子靶点:近期亮点与未来展望

Dilpreet Kaur, Shamsher Singh
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引用次数: 0

摘要

帕金森病(Parkinson's disease,PD)是一种与年龄相关的进行性神经退行性疾病,其特征是大脑黑质下部(substantia nigra pars compacta,SNpc)多巴胺能神经元的丧失。越来越多的证据表明,细胞凋亡、神经炎症、线粒体功能障碍和氧化应激是帕金森病发病机制中的重要因素。异槲皮素是一种天然黄烷醇化合物,具有抗凋亡、抗炎、抗氧化和神经保护作用。异槲皮素还能调节各种信号通路,如Rhosignaling级联、Nrf-2、TLR4、NF-κB、MAPK、Bcl-2、Bax蛋白,这些都是众所周知的导致疾病进展的原因。这些通路参与了细胞平衡、促炎细胞因子转录、氧化应激、小胶质细胞活化和凋亡通路的调节。在这篇综述中,我们重点介绍了上述途径的机制,以及通过类黄酮化合物异槲皮素以各种方式对其进行调节的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Isoquercetin Neuroprotective Molecular Targets in Parkinson’s Disease: Recent Highlights and Future Perspectives
Parkinson's disease (PD) is an age-related progressive neurodegenerative condition characterized by dopaminergic neuronal loss in the brain's substantia nigra pars compacta (SNpc). Growing evidence suggests that apoptosis, neuroinflammation, mitochondrial dysfunction, and oxidative stress are important factors in the pathogenesis of Parkinson's disease. Isoquercetin is a natural flavanol compound possessing anti-apoptotic, anti-inflammatory, anti-oxidant, and neuroprotective activities. Isoquercetin also has the capability to modulate various signaling pathways such as Rho signaling cascade, Nrf-2, TLR4, NF-κB, MAPK, Bcl-2, Bax proteins, which are well-known causes for the progression of the disease. These pathways are involved in cellular homeostasis, transcription of proinflammatory cytokines, oxidative stress, microglial activation, and regulation of the apoptotic pathways. In this review, we have highlighted the mechanisms of the above-mentioned pathways and their modulation via the flavonoid compound isoquercetin in various ways.
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