{"title":"评估肠道微生物对帕金森病的神经保护作用:体内和体外方法。","authors":"Kanika Bhardwaj, Neelu Kanwar Rajawat, Nupur Mathur, Aviral Kaushik","doi":"10.1007/s12017-024-08799-w","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Evaluation of Neuroprotective Effect of Gut Microbe in Parkinson's Disease: An In Silico and In Vivo Approach.\",\"authors\":\"Kanika Bhardwaj, Neelu Kanwar Rajawat, Nupur Mathur, Aviral Kaushik\",\"doi\":\"10.1007/s12017-024-08799-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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. 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引用次数: 0
摘要
帕金森病是一种以大脑黑质区域多巴胺能神经元死亡为特征的进行性神经退行性疾病。α-突触核蛋白(α-synuclein)的聚集是导致帕金森病发病的一个因素。本研究的目的是利用硅学和体内方法研究肠道微生物对α-突触核蛋白聚集的神经保护作用。我们重点研究了α-突触核蛋白与肠道细菌释放的代谢物之间的相互作用,这些代谢物可防止帕金森病。我们采用了三种针对α-突触核蛋白蛋白的益生微生物菌株:所选的 PDB ID 分别为二氢叶酸还原酶(3DFR)、蛋氨酸合成酶(6BM5)和色氨酸-tRNA 合成酶(3PRH)。我们使用 HEX Dock 6.0 软件研究了这些蛋白质之间的相互作用。在各种代谢物中,由大肠杆菌产生的蛋氨酸合成酶显示出与α-突触核蛋白的潜在相互作用。为了进一步评估大肠杆菌的神经保护作用,我们使用鱼藤酮诱导的帕金森病小鼠模型进行了一项体内研究。通过行为测试评估了动物的运动功能,还检测了氧化应激和神经递质水平。结果表明,与鱼藤酮诱导的帕金森病小鼠模型相比,用大肠杆菌治疗的小鼠的神经变性率大大降低。此外,组织病理学研究也证明了大肠杆菌对神经的保护作用。总之,这项研究为今后的研究奠定了基础,表明肠道细菌可作为潜在的治疗剂,用于开发治疗帕金森病的药物。 图 1.
Evaluation of Neuroprotective Effect of Gut Microbe in Parkinson's Disease: An In Silico and In Vivo Approach.
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.