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Clostridium butyricum exerts a neuroprotective effect in a mouse model of traumatic brain injury via the gut‐brain axis
Author(s) -
Li H.,
Sun J.,
Du J.,
Wang F.,
Fang R.,
Yu C.,
Xiong J.,
Chen W.,
Lu Z.,
Liu J.
Publication year - 2018
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.13260
Subject(s) - occludin , neuroprotection , traumatic brain injury , protein kinase b , blood–brain barrier , brain damage , medicine , neurodegeneration , tight junction , intestinal permeability , downregulation and upregulation , endocrinology , pharmacology , chemistry , biology , central nervous system , apoptosis , microbiology and biotechnology , biochemistry , disease , psychiatry , gene
Abstract Background Traumatic brain injury (TBI) is a common occurrence following gastrointestinal dysfunction. Recently, more and more attentions are being focused on gut microbiota in brain and behavior. Glucagon‐like peptide‐1 (GLP‐1) is considered as a mediator that links the gut‐brain axis. The aim of this study was to explore the neuroprotective effects of Clostridium butyricum (Cb) on brain damage in a mouse model of TBI. Methods Male C57BL/6 mice were subjected to a model of TBI‐induced by weight‐drop impact head injury and were treated intragastrically with Cb. The cognitive deficits, brain water content, neuronal death, and blood‐brain barrier (BBB) permeability were evaluated. The expression of tight junction (TJ) proteins, Bcl‐2, Bax, GLP‐1 receptor (GLP‐1R), and phosphorylation of Akt (p‐Akt) in the brain were also measured. Moreover, the intestinal barrier permeability, the expression of TJ protein and GLP‐1, and IL‐6 level in the intestine were detected. Results Cb treatment significantly improved neurological dysfunction, brain edema, neurodegeneration, and BBB impairment. Meanwhile, Cb treatment also significantly increased the expression of TJ proteins (occludin and zonula occluden‐1), p‐Akt and Bcl‐2, but decreased expression of Bax. Moreover, Cb treatment exhibited more prominent effects on decreasing the levels of plasma d ‐lactate and colonic IL‐6, upregulating expression of Occludin, and protecting intestinal barrier integrity. Furthermore, Cb‐treated mice showed increased the secretion of intestinal GLP‐1 and upregulated expression of cerebral GLP‐1R. Conclusions Our findings demonstrated the neuroprotective effect of Cb in TBI mice and the involved mechanisms were partially attributed to the elevating GLP‐1 secretion through the gut‐brain axis.