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Lactobacillus plantarum J26 Alleviating Alcohol-Induced Liver Inflammation by Maintaining the Intestinal Barrier and Regulating MAPK Signaling Pathways

Alcoholic liver disease (ALD), as a global health problem, is mainly caused by liver inflammation. Meanwhile, probiotics have been considered as a potential and promising strategy to prevent and alleviate ALD. This study aimed to investigate the ameliorative effect of pre-intaking with Lactobacillus...

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Detalles Bibliográficos
Autores principales: Li, Hongxuan, Cheng, Shasha, Huo, Jiacheng, Dong, Kai, Ding, Yixin, Man, Chaoxin, Zhang, Yu, Jiang, Yujun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9824527/
https://www.ncbi.nlm.nih.gov/pubmed/36615846
http://dx.doi.org/10.3390/nu15010190
Descripción
Sumario:Alcoholic liver disease (ALD), as a global health problem, is mainly caused by liver inflammation. Meanwhile, probiotics have been considered as a potential and promising strategy to prevent and alleviate ALD. This study aimed to investigate the ameliorative effect of pre-intaking with Lactobacillus plantarum J26 (L. plantarum J26) on alcohol-induced liver inflammation, with emphasis on the underlying mechanism for alleviating ALD. The results indicated that L. plantarum J26 could reduce the abundance of Gram-negative pathogenic bacteria by regulating the gut microbiota in mice with alcoholic liver injury, thereby reducing the lipopolysaccharide (LPS) content in the intestine. In addition, L. plantarum J26 could also maintain the intestinal barrier, prevent LPS from crossing the intestinal barrier to correct disorders of the gut–liver axis and then inhibit the activation of Toll-like receptor 4 (TLR4)-mediated MAPK signaling pathway, reducing liver inflammation and restoring liver functions. In conclusion, pre-intake of L. plantarum J26 could alleviate alcohol-induced liver inflammation, which may be closely related to the role of intestinal microbiota in regulating and maintaining the intestinal barrier and then regulating the MAPK signaling pathway.