Protective Mechanism of Lactobacillus plantarum KFY02 Preventing CCl₄-Induced Liver Injury by Transforming Geniposide into Genipin to Boost Antioxidant Defence
Résumé fourni par la source
Lactobacillus plantarum belongs to the genus Lactobacillus and is a lactic acid bacterium commonly found in the fermented products of milk, meat, and many vegetables. It can pass through the stomach and colonise the intestine to play a beneficial role. L. plantarum has a wide range of applications in various diseases, but there are few reports on its role in liver injury and as an antioxidant. This study investigated the mechanism by which Lactobacillus plantarum KFY02 (KFY02) alleviates CCl₄-induced liver injury in mice, focusing on its role in enhancing systemic antioxidant capacity through the bioconversion of geniposide to genipin. Experimental results confirmed that KFY02 partially converts geniposide into genipin in vitro. In the mouse model of liver injury, both KFY02 and geniposide significantly reduced the liver index and decreased serum levels of AST, ALT, TG, MDA, and the pro-inflammatory cytokines IL-6, IL-12, TNF-α, and IFN-γ, while up-regulating the activity of antioxidant enzymes SOD and GSH-Px. At the molecular level, KFY02 and geniposide up-regulated the mRNA and protein expression of Mn-SOD, Cu/Zn-SOD, CAT, GSH-Px, and IκB-α, and down-regulated the expression of COX-2, iNOS, and NF-κB in liver tissues. In summary, L. plantarum KFY02 mitigates CCl₄-induced hepatic damage by potentiating the body's antioxidant defences, an effect mediated through the microbial conversion of geniposide to its more active form, genipin.
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Contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Protective Mechanism of Lactobacillus plantarum KFY02 Preventing CCl₄-Induced Liver Injury by Transforming Geniposide into Genipin to Boost Antioxidant Defence
- Date Crossref
- 02/02/2026
- Éditeur
- BP International
- Type
- book-chapter
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude et ne compte pas comme une seconde source scientifique indépendante.
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