尼古丁在秀丽隐杆线虫帕金森病模型中调节氧化和线粒体通路的治疗潜力

IF 2.9 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Inam Ullah, Shahab Uddin, Wang Xin, Hongyu Li
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引用次数: 0

摘要

背景帕金森病(PD)是影响老年人中枢神经系统(CNS)的最广泛的神经退行性疾病之一。到目前为止,还没有公认的治疗这种疾病的方法。帕金森氏症的发展不是因为新的药物。生物活性植物化学物质是一种天然替代品,可以帮助老年人延缓与年龄有关的认知疾病。目前,fda批准的帕金森病药物仅提供症状缓解。本研究试图确定尼古丁,一种在茄属植物,特别是烟草中天然发现的生物碱,是否可以减少秀丽隐杆线虫病模型中的帕金森病。方法采用不同于野生型的线虫模型,分析尼古丁的抗氧化和修复线粒体功能障碍潜能及其相关的神经保护作用。我们使用隐杆线虫模型研究了尼古丁对氧化应激耐受性和相关调控途径的影响。结果野生型秀丽隐杆线虫经尼古丁处理后,其氧化应激存活率高于对照组。尼古丁降低秀丽隐杆线虫细胞内活性氧水平。此外,尼古丁增加了SOD、CAT和MDA的水平以及与应激反应相关的基因gst-4、hsf-6和hsf-1的表达,以及线粒体功能基因mev-1、isp-1和cox-4的表达。最后,我们的分子分析表明,尼古丁的抗氧化作用是通过皮肤-1调节介导的。施用百草枯后,尼古丁治疗也导致ATP和MMP水平升高。结论本研究阐明了尼古丁体内抗氧化活性的多种作用机制和通讯途径,为其在神经退行性疾病的潜在治疗应用提供了坚实的药理学基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
"Therapeutic Potential of Nicotine in Modulating Oxidative and Mitochondrial Pathways in a C. elegans Parkinson's Disease Model".

BackgroundParkinson's disease (PD) is one of the most widespread neurodegenerative diseases that affect the central nervous system (CNS) in elderly individuals. As of right now, there is no recognized cure for this illness. Parkinson's disease is not developing because of new medications. Bioactive phytochemicals are a natural alternative that can help older persons postpone age-related cognitive diseases.PurposeCurrently, FDA-licensed medicines for Parkinson's disease only provide symptomatic relief. This study attempts to establish whether nicotine, an alkaloid found naturally in nightshade plants, especially tobacco, may diminish parkinsonism in a model of Caenorhabditis elegans disease.MethodsThis study analyzes the antioxidant and restorative mitochondrial dysfunction potential of nicotine and its related neuroprotective benefits by utilizing models of Caenorhabditis worm strains that are different from the wild type. We examined the effects of nicotine on oxidative stress tolerance and associated regulatory pathways using a model of Caenorhabditis worms.ResultsOur results showed that wild-type C. elegans treated with nicotine had higher survival rates during oxidative stress caused by Juglone than those treated with the control. Nicotine decreased intracellular reactive oxygen species levels in C. elegans. In addition, nicotine increased levels of SOD, CAT, and MDA as well as the expression of genes related to stress response, including gst-4, hsf-6, and hsf-1, and mitochondrial function genes, including mev-1, isp-1, and cox-4. Finally, our molecular analysis indicates that the anti-oxidative effects of nicotine are mediated via skin-1 modulation. After Paraquat was administered, nicotine therapy also resulted in higher levels of ATP and MMP.ConclusionOur research clarifies the various mechanisms of action and communication pathways that underlie nicotine's antioxidant activity in vivo, offering a solid pharmacological foundation for its potential therapeutic use in neurodegeneration.

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来源期刊
Free Radical Research
Free Radical Research 生物-生化与分子生物学
CiteScore
6.70
自引率
0.00%
发文量
47
审稿时长
3 months
期刊介绍: Free Radical Research publishes high-quality research papers, hypotheses and reviews in free radicals and other reactive species in biological, clinical, environmental and other systems; redox signalling; antioxidants, including diet-derived antioxidants and other relevant aspects of human nutrition; and oxidative damage, mechanisms and measurement.
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