Lactobacillus paracasei CCFM1223 Protects against Lipopolysaccharide-Induced Acute Liver Injury in Mice by Regulating the "Gut-Liver" Axis.
Microorganisms
; 10(7)2022 Jun 30.
Article
em En
| MEDLINE
| ID: mdl-35889040
ABSTRACT
BACKGROUND:
Lactobacillus paracasei CCFM1223, a probiotic previously isolated from the healthy people's intestine, exerts the beneficial influence of preventing the development of inflammation.METHODS:
The aim of this research was to explore the beneficial effects of L. paracasei CCFM1223 to prevent lipopolysaccharide (LPS)-induced acute liver injury (ALI) and elaborate on its hepatoprotective mechanisms.RESULTS:
L. paracasei CCFM1223 pretreatment remarkably decreased the activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in mice with LPS treatment and remarkably recovered LPS-induced the changes in inflammatory cytokines (tumor necrosis factor-α (TNF-α), transforming growth factor-ß (TGF-ß), interleukin (IL)-1ß, IL-6, IL-17, IL-10, and LPS) and antioxidative enzymes activities (total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT)). Metagenomic analysis showed that L. paracasei CCFM1223 pretreatment remarkably increased the relative abundance of Catabacter compared with the LPS group but remarkably reduced the relative abundance of [Eubacterium] xylanophilumgroup, ASF356, LachnospiraceaeNK4A136group, and Lachnoclostridium, which is closely associated with the inflammation cytokines and antioxidative enzymes. Furthermore, L. paracasei CCFM1223 pretreatment remarkably increased the colonic, serum, and hepatic IL-22 levels in ALI mice. In addition, L. paracasei CCFM1223 pretreatment remarkably down-regulated the hepatic Tlr4 and Nf-kß transcriptions and significantly up-regulated the hepatic Tlr9, Tak1, Iκ-Bα, and Nrf2 transcriptions in ALI mice.CONCLUSIONS:
L. paracasei CCFM1223 has a hepatoprotective function in ameliorating LPS-induced ALI by regulating the "gut-liver" axis.
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MEDLINE
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article