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牛磺酸纳米颗粒对鱼藤酮诱导的小鼠帕金森病的神经保护作用

Neuroprotective Impacts of Taurine Nanoparticles Against Rotenone Induced Parkinson's Disease in Mice.

作者信息

Beltagy Doha M, Elgindy Khaled M, Mohamed Tarek M, Tousson Ehab, Izzularab Batoul M

机构信息

Biochemistry Department, Faculty of Science, Damanhour University, Egypt.

Biochemistry Division, Chemistry Department, Faculty of Science, Tanta University, Egypt.

出版信息

Toxicol Mech Methods. 2025 Aug 13:1-26. doi: 10.1080/15376516.2025.2547874.

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder affects motor and cognitive functions in patients. The main pathology of this illness is the loss of dopaminergic neurons in the substantia nigra which leads to locomotor impairment such as tremors, bradykinesia, and muscular rigidity. In late stages of PD, non-motor symptoms like cognitive deficits develop, affecting the life quality. Recent studies indicated that these non-motor symptoms are attributed to neuronal loss in the hippocampus and impaired neurotransmission, due to oxidative stress and neuroinflammation. This study aimed to evaluate the antioxidant and anti-inflammatory effects of Taurine (TRN) and taurine nanoparticles (TRN-NPs) and investigate their role in improving hippocampal neuronal survival and their synergistic effects with Sinemet tablets as a dopamine agonist, on rotenone-induced PD experimental mice model. The experiment involved 70 mice categorized into G1:control, G2:Sinemet (reference drug), G3:TRN-control, G4:TRN-NPs-control, G5:Rotenone (PD model), G6: Rotenone + Sinemet, G7:Rotenone + TRN, G8:Rotenone + TRN-NPs, G9:Rotenone + Sinemet + TRN and G10:Rotenone + Sinemet + TRN-NPs. At the experiment end, Behavioral parameter was defined using inverted screen test and various assessments. Neurotransmitters, oxidative stress biomarkers, pro-inflammatory cytokines, brain-derived neurotrophic factor (BDNF), micro-RNA 214, and micro-RNA 216a were evaluated. Treatment with TRN or TRN-NPs alone or with Sinemet alleviate oxidative stress, neuroinflammation and hippocampal neurodegeneration, enhance neurotransmission, neuronal survival and protection against cellular death. These results were confirmed by histological and immunohistochemical studies. The results suggest that TRN-NPs represent an innovative adjunct supplement to traditional dopaminergic therapies, improve neuroprotection, increased bioavailability, addressing current limitations in drug delivery and therapeutic efficacy thus opening up promising therapeutic approaches for PD management.

摘要

帕金森病(PD)是一种进行性神经退行性疾病,会影响患者的运动和认知功能。该疾病的主要病理学特征是黑质中多巴胺能神经元的丧失,这会导致运动障碍,如震颤、运动迟缓及肌肉僵硬。在帕金森病晚期,会出现认知缺陷等非运动症状,影响生活质量。最近的研究表明,这些非运动症状归因于海马体中的神经元丧失以及由于氧化应激和神经炎症导致的神经传递受损。本研究旨在评估牛磺酸(TRN)和牛磺酸纳米颗粒(TRN-NPs)的抗氧化和抗炎作用,并研究它们在改善海马体神经元存活方面的作用,以及它们与作为多巴胺激动剂的息宁片协同作用于鱼藤酮诱导的帕金森病实验小鼠模型的效果。实验涉及70只小鼠,分为G1:对照组;G2:息宁(参比药物)组;G3:TRN对照组;G4:TRN-NPs对照组;G5:鱼藤酮(帕金森病模型)组;G6:鱼藤酮 + 息宁组;G7:鱼藤酮 + TRN组;G8:鱼藤酮 + TRN-NPs组;G9:鱼藤酮 + 息宁 + TRN组;G10:鱼藤酮 + 息宁 + TRN-NPs组。在实验结束时,使用倒屏试验和各种评估来定义行为参数。对神经递质、氧化应激生物标志物、促炎细胞因子、脑源性神经营养因子(BDNF)、微小RNA 214和微小RNA 216a进行了评估。单独使用TRN或TRN-NPs或与息宁联合治疗可减轻氧化应激、神经炎症和海马体神经退行性变,增强神经传递、神经元存活并保护细胞免于死亡。这些结果通过组织学和免疫组织化学研究得到证实。结果表明,TRN-NPs是传统多巴胺能疗法的一种创新辅助补充剂,可改善神经保护作用、提高生物利用度,解决当前药物递送和治疗效果方面的局限性,从而为帕金森病的管理开辟了有前景的治疗方法。

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