国内团队:丁酸梭菌或可通过诱导GLP-1表达缓解帕金森
创作:nana 审核:nana 2020年12月26日
  • 用1-甲基-4-苯基- 1,2,3,6 -四氢吡啶诱导雄性C57BL/6小鼠,建立帕金森病(PD)模型;
  • 柱杆试验、梁行走试验、强迫游泳试验等检测表明,丁酸梭菌(Cb)干预可改善PD小鼠的运动功能、减少多巴胺神经元丢失、改善突触功能障碍及抑制小胶质细胞激活;
  • 还能促进PD小鼠肠道菌群恢复稳态,提高PD小鼠结肠胰高血糖素样蛋白GLP-1、结肠G蛋白偶联受体GPR41/43和大脑GLP-1受体水平;
  • 提示Cb对帕金森病的缓解或与改善异常肠道微生物-肠-脑轴有关。
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nana
肠道菌群失调可能是帕金森病的一个风险因素,并且最近研究表明丁酸梭菌靶向干预,可通过调节微生物-肠-脑轴,显示出对帕金森病治疗的良好效果,但丁酸梭菌对帕金森的潜在有益作用及其机制尚不清楚。Brain Behavior and Immunity近期发表了来自国内团队的文章,探讨了其中的可能机制。给帕金森疾病模型小鼠连续灌胃四周丁酸梭菌(5 × 108 CFU/天),检测小鼠运动功能、多巴胺能神经元丢失、突触可塑性、小胶质细胞激活,以及结肠胰高血糖素样肽-1 (GLP-1)、结肠G蛋白偶联受体GPR41/43和大脑GLP-1受体水平及肠道菌群结构变化,结果表明,丁酸梭菌可能通过调节肠道菌群-肠-脑轴,缓解帕金森疾病。
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Probiotic Clostridium butyricum ameliorated motor deficits in a mouse model of Parkinson’s disease via gut microbiota-GLP-1 pathway

益生菌丁酸梭菌通过肠道微生物-GLP-1途径改善帕金森病小鼠模型的运动障碍

10.1016/j.bbi.2020.10.014

2020-10-24, Article

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A connection between gut microbiota and Parkinson’s disease (PD) indicates that dysbiosis of the gut microbiota might represent a risk factor for PD. Microbiota-targeted interventions, including probiotic Clostridium butyricum (Cb), have been recently shown to have favorable effects in PD by regulating microbiota-gut-brain axis. However, the potential beneficial roles and its mechanisms of Cb on PD were still unknown. Male C57BL/6 mice were subjected to a PD model-induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) and were treated intragastrically with Cb for 4 weeks. The motor functions were assessed by a series of behavioral tests including pole test, beam walking teat, forced swimming test and open field test. The dopaminergic neuron loss, synaptic plasticity and microglia activation, as well as the levels of colonic glucagon-like peptide-1 (GLP-1), colonic G protein-coupled receptors GPR41/43 and cerebral GLP-1 receptors were assessed. Gut microbial composition was assessed by 16S rRNA sequencing analysis. Our results showed that oral administration of Cb could improve motor deficits, dopaminergic neuron loss, synaptic dysfunction and microglia activation in the MPTP-induced mice. Meanwhile, Cb treatment could reverse the dysbiosis of gut microbiota and the decreased levels of colonic GLP-1, colonic GPR41/43 and cerebral GLP-1 receptor in the MPTP-induced mice. These findings indicated that the neuroprotective mechanism of Cb on PD might be related to the improvement of abnormal gut microbiota-gut-brain axis.

First Authors:
Jing Sun,Haijun Li

Correspondence Authors:
Zongxin Ling,Jiaming Liu

All Authors:
Jing Sun,Haijun Li,Yangjie Jin,Jiaheng Yu,Shiyin Mao,Kuan-Pin Su,Zongxin Ling,Jiaming Liu

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