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Lactobacillus plantarum PS128 alleviates neurodegenerative progression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models of Parkinson’s disease
Brain, Behavior, and Immunity ( IF 8.8 ) Pub Date : 2020-11-01 , DOI: 10.1016/j.bbi.2020.07.036
Jian-Fu Liao , Yun-Fang Cheng , Shu-Ting You , Wen-Chun Kuo , Chi-Wei Huang , Jen-Jie Chiou , Chih-Chieh Hsu , Hsiu-Mei Hsieh-Li , Sabrina Wang , Ying-Chieh Tsai

Evidence suggests that the Parkinson's disease (PD) pathogenesis is strongly associated with bidirectional pathways in the microbiota-gut-brain axis (MGBA), and psychobiotics may inhibit PD progression. We previously reported that the novel psychobiotic strain, Lactobacillus plantarum PS128 (PS128), ameliorated abnormal behaviors and modulated neurotransmissions in dopaminergic pathways in rodent models. Here, we report that orally administering PS128 for 4 weeks significantly alleviated the motor deficits, elevation in corticosterone, nigrostriatal dopaminergic neuronal death, and striatal dopamine reduction in 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced PD mouse models. PS128 ingestion suppressed glial cell hyperactivation and increased norepinephrine and neurotrophic factors in the striatum of the PD-model mice. PS128 administration also attenuated MPTP-induced oxidative stress and neuroinflammation in the nigrostriatal pathway. Fecal analysis showed that PS128 modulated the gut microbiota. L. plantarum abundance was significantly increased along with methionine biosynthesis-related microbial modules. PS128 also suppressed the increased family Enterobacteriaceae and lipopolysaccharide and peptidoglycan biosynthesis-related microbial modules caused by MPTP. In conclude, PS128 ingestion alleviated MPTP-induced motor deficits and neurotoxicity.PS128 supplementation inhibited neurodegenerative processes in PD-model mice and may help prevent PD.

中文翻译:

植物乳杆菌 PS128 减轻 1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的帕金森病小鼠模型的神经退行性进展

有证据表明,帕金森病 (PD) 的发病机制与微生物群-肠-脑轴 (MGBA) 的双向通路密切相关,精神生物素可能会抑制 PD 的进展。我们之前报道过,新型精神生物菌株植物乳杆菌 PS128 (PS128) 改善了啮齿动物模型中多巴胺能通路的异常行为和调节神经传递。在这里,我们报告口服 PS128 4 周显着减轻运动缺陷、皮质酮升高、黑质纹状体多巴胺能神经元死亡和纹状体多巴胺减少 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP) ) 诱导的 PD 小鼠模型。PS128 的摄入抑制了 PD 模型小鼠纹状体中的神经胶质细胞过度活化并增加了去甲肾上腺素和神经营养因子。PS128 给药还减弱了 MPTP 诱导的黑质纹状体通路中的氧化应激和神经炎症。粪便分析表明,PS128 调节肠道微生物群。L. plantarum 丰度随着蛋氨酸生物合成相关的微生物模块显着增加。PS128 还抑制了由 MPTP 引起的肠杆菌科、脂多糖和肽聚糖生物合成相关微生物模块的增加。总之,摄入 PS128 减轻了 MPTP 诱导的运动缺陷和神经毒性。补充 PS128 抑制了 PD 模型小鼠的神经退行性过程,并可能有助于预防 PD。随着蛋氨酸生物合成相关微生物模块的出现,植物群丰度显着增加。PS128 还抑制了由 MPTP 引起的肠杆菌科和脂多糖和肽聚糖生物合成相关微生物模块的增加。总之,摄入 PS128 减轻了 MPTP 诱导的运动缺陷和神经毒性。补充 PS128 抑制了 PD 模型小鼠的神经退行性过程,并可能有助于预防 PD。随着蛋氨酸生物合成相关微生物模块的出现,植物群丰度显着增加。PS128 还抑制了由 MPTP 引起的肠杆菌科、脂多糖和肽聚糖生物合成相关微生物模块的增加。总之,摄入 PS128 减轻了 MPTP 诱导的运动缺陷和神经毒性。补充 PS128 抑制了 PD 模型小鼠的神经退行性过程,并可能有助于预防 PD。
更新日期:2020-11-01
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