期刊
BRAIN RESEARCH BULLETIN
卷 187, 期 -, 页码 111-121出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2022.06.013
关键词
Enteric glia; Parkinson?s disease model; Inflammation; Intestinal epithelial barrier; Gut -brain axis
资金
- Funda?a?o Carlos Chagas Filho de Amparo a`Pesquisa do Estado do Rio de Janeiro (FAPERJ) , Brazil - Grant [E-26/210.023/2018, E-26/210.878/2014, E-26/202925/2019, 001, IC210613, 304414/2018-2]
- Fundaao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ) , Brazil [E-26/210.023/2018, E-26/210.878/2014, E-26/202925/2019]
- Coordenaao de Aperfeioamento de Pessoal de Nvel Superior (CAPES) , Brazil [001]
- Pro-Reitoria de Pesquisa, Pos-graduaao e Inovaao (PROPPI) , Brazil [IC210613]
- Conselho Nacional de Desenvolvimento Cientfico e Tecnologico (CNPq) , Brazil [304414/2018-2]
- CAPES fellowship
Enteric glial cells may serve as an early enteric signal in Parkinson's disease, accompanied by inflammation and motor dysfunction.
Enteric glial cells (EGCs) constitute the majority of the neural population of the enteric nervous system and are found in all layers of the gastrointestinal tract. It is active in enteric functions such as immunomodulation, participating in inflammation and intestinal epithelial barrier (IEB) regulation. Both EGCs and IEB have been described as altered in Parkinson's disease (PD). Using an animal model of PD induced by 6-hydroxydopamine (6-OHDA), we investigated the effect of ongoing neurodegeneration on EGCs and inflammatory response during short periods after model induction. C57Bl/6 male mice were unilaterally injected with 6-OHDA in the striatum. Compared to the control group, 6-OHDA animals showed decreased relative water content in their feces from 1 w after model induction. Moreover, at 1 and 2 w post-induction, groups showed histopathological changes indicative of intestinal inflammation. We identified an increase in IBA1 and GFAP levels in the intestinal mucosa. At an earlier survival of 48 h, we detected an increase in GFAP in the neuromuscular layer, suggesting that it was a primary event for the upregulation of GDNF, TNF-alpha, and occludin in the intestinal mucosa observed after 1 w. Within 2 w, we identified a decrease in the expression of occludin barrier proteins. Thus, EGCs modulation may be an early enteric signal induced by parkinsonian neurodegeneration, followed by inflammatory and dysmo-tility signs besides IEB modification.
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