Probiotic Clostridium butyricum ameliorated motor deficits in a mouse model of Parkinson’s disease via gut microbiota-GLP-1 pathway

Nov 5, 2020Brain, behavior, and immunity

Probiotic Clostridium butyricum improved movement problems in mice with Parkinson's disease through gut bacteria and GLP-1 pathway

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Abstract

Oral administration of probiotic Clostridium butyricum for 4 weeks improved motor deficits and dopaminergic neuron loss in a Parkinson's disease model in mice.

Dysbiosis of gut microbiota may represent a risk factor for Parkinson's disease.
Clostridium butyricum treatment improved motor functions and reduced dopaminergic neuron loss in mice subjected to a Parkinson's disease model.
Treatment with Cb reversed dysbiosis of gut microbiota and increased levels of colonic glucagon-like peptide-1 and G protein-coupled receptors.
The neuroprotective mechanism of Cb may be linked to the improvement of the gut microbiota-gut-brain axis.

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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.

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Probiotic Clostridium butyricum ameliorated motor deficits in a mouse model of Parkinson’s disease via gut microbiota-GLP-1 pathway

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