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基于计算和实验的方法评价肠道微生物对帕金森病的神经保护作用。

Evaluation of Neuroprotective Effect of Gut Microbe in Parkinson's Disease: An In Silico and In Vivo Approach.

机构信息

Department of Zoology, IIS (Deemed to be University), Jaipur, Rajasthan, 302020, India.

Department of Zoology, University of Rajasthan, Jaipur, Rajasthan, 302020, India.

出版信息

Neuromolecular Med. 2024 Aug 1;26(1):32. doi: 10.1007/s12017-024-08799-w.

Abstract

Parkinson's disease is a progressive neurodegenerative disorder marked by the death of dopaminergic neurons in the substantia nigra region of the brain. Aggregation of alpha-synuclein (α-synuclein) is a contributing factor to Parkinson's disease pathogenesis. The objective of this study is to investigate the neuroprotective effects of gut microbes on α-synuclein aggregation using both in silico and in vivo approaches. We focussed on the interaction between α-synuclein and metabolites released by gut bacteria that protect from PD. We employed three probiotic microbe strains against α-synuclein protein: Lactobacillus casei, Escherichia coli, and Bacillus subtilis, with their chosen PDB IDs being Dihydrofolate reductase (3DFR), methionine synthetase (6BM5), and tryptophanyl-tRNA synthetase (3PRH), respectively. Using HEX Dock 6.0 software, we examined the interactions between these proteins. Among the various metabolites, methionine synthetase produced by E. coli showed potential interactions with α-synuclein. To further evaluate the neuroprotective benefits of E. coli, an in vivo investigation was performed using a rotenone-induced Parkinsonian mouse model. The motor function of the animals was assessed through behavioural tests, and oxidative stress and neurotransmitter levels were also examined. The results demonstrated that, compared to the rotenone-induced PD mouse model, the rate of neurodegeneration was considerably reduced in mice treated with E. coli. Additionally, histopathological studies provided evidence of the neuroprotective effects of E. coli. In conclusion, this study lays the groundwork for future research, suggesting that gut bacteria may serve as potential therapeutic agents in the development of medications to treat Parkinson's disease. fig. 1.

摘要

帕金森病是一种进行性神经退行性疾病,其特征是大脑黑质区域的多巴胺能神经元死亡。α-突触核蛋白(α-synuclein,α-syn)的聚集是帕金森病发病机制的一个促成因素。本研究旨在通过体内和体外方法研究肠道微生物对 α-syn 聚集的神经保护作用。我们专注于α-syn 与肠道细菌释放的保护 PD 的代谢物之间的相互作用。我们使用了三种益生菌微生物菌株来对抗 α-syn 蛋白:干酪乳杆菌、大肠杆菌和枯草芽孢杆菌,它们的选择 PDB ID 分别为二氢叶酸还原酶(3DFR)、甲硫氨酸合成酶(6BM5)和色氨酰-tRNA 合成酶(3PRH)。使用 HEX Dock 6.0 软件,我们检查了这些蛋白质之间的相互作用。在各种代谢物中,大肠杆菌产生的甲硫氨酸合成酶显示出与 α-syn 潜在的相互作用。为了进一步评估大肠杆菌的神经保护益处,我们使用鱼藤酮诱导的帕金森病小鼠模型进行了体内研究。通过行为测试评估动物的运动功能,还检查了氧化应激和神经递质水平。结果表明,与鱼藤酮诱导的 PD 小鼠模型相比,用大肠杆菌处理的小鼠神经退行性病变的速度明显降低。此外,组织病理学研究提供了大肠杆菌具有神经保护作用的证据。总之,本研究为未来的研究奠定了基础,表明肠道细菌可能成为治疗帕金森病药物开发的潜在治疗剂。图 1.

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