Institute of Biochemistry and Molecular Biology, National Yang-Ming University, 155, Section 2, Linong Street, Beitou Dist., Taipei City 11221, Taiwan, ROC.
Institute of Biochemistry and Molecular Biology, National Yang-Ming University, 155, Section 2, Linong Street, Beitou Dist., Taipei City 11221, Taiwan, ROC; Microbiome Research Center, National Yang-Ming University, 155, Section 2, Linong Street, Beitou Dist., Taipei City 11221, Taiwan, ROC; Bened Biomedical Co. Ltd., 2F-2, No.129, Sec. 2, Zhongshan N. Rd., Zhongshan Dist., Taipei City 104, Taiwan, ROC.
Brain Behav Immun. 2020 Nov;90:26-46. doi: 10.1016/j.bbi.2020.07.036. Epub 2020 Jul 30.
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.
有证据表明,帕金森病(PD)的发病机制与微生物群-肠道-大脑轴(MGBA)中的双向途径密切相关,而益生菌可能会抑制 PD 的进展。我们之前报道过,新型益生菌菌株植物乳杆菌 PS128(PS128)可改善啮齿动物模型中异常行为,并调节多巴胺能通路中的神经递质传递。在这里,我们报告称,口服 PS128 4 周可显著缓解运动功能障碍、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,这些是 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的 PD 小鼠模型中的作用。PS128 摄入可抑制小胶质细胞过度激活,并增加 PD 模型小鼠纹状体中的去甲肾上腺素和神经营养因子。PS128 给药还可减轻 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 可调节肠道微生物群。植物乳杆菌的丰度显着增加,伴随着蛋氨酸生物合成相关的微生物模块。PS128 还抑制了 MPTP 引起的肠杆菌科家族和脂多糖及肽聚糖生物合成相关微生物模块的增加。总之,PS128 的摄入可缓解 MPTP 诱导的运动功能障碍和神经毒性。PS128 的补充抑制了 PD 模型小鼠的神经退行性过程,可能有助于预防 PD。
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