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Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
Published on: February 10, 2015
Exogenous Low-Molecular-Weight Collagen Bioactive Peptides Alleviate Cholestatic Liver Fibrosis in Mice by Modulating
Shuxia Cao1, Lina Ma1, Jiaqi Huo1
1Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji 133002, China.
Abstract:
Exogenous low-molecular-weight collagen bioactive peptides (CP) derived from codfish skin have demonstrated anti-inflammatory and antifibrotic effects. However, the roles of CP in protecting against cholestatic liver fibrosis remain unclear. This study aimed to evaluate the effects of CP on cholestatic liver fibrosis. A bile duct ligation (BDL) model was employed, and the effects of CP on liver fibrosis in BDL mice were assessed. Proteomics was used to identify the targets and signaling pathways of the CP. 16S rRNA sequencing was performed to evaluate the effects of CP on the gut microbiota diversity. CP alleviated bile stasis, liver inflammation, oxidative stress, hepatocyte apoptosis, and liver fibrosis. Proteomics and molecular biology revealed that CP targeted cell adhesion molecules (CAMs), thereby inhibiting the Wnt/β-catenin signaling pathway. 16S rRNA sequencing demonstrated that CP restored gut microbiota homeostasis. CP alleviates cholestatic liver fibrosis in mice by modulating CAMs to inhibit Wnt/β-catenin signaling and restore gut microbiota homeostasis.
Insights
Codfish skin collagen peptides (CP) alleviate cholestatic liver fibrosis by reducing inflammation and fibrosis. CP targets cell adhesion molecules, inhibits Wnt/β-catenin signaling, and restores gut microbiota balance.
Area of Science:
- Hepatology
- Gastroenterology
- Molecular Biology
Background:
- Cholestatic liver fibrosis is a progressive condition with limited treatment options.
- Exogenous low-molecular-weight collagen bioactive peptides (CP) from codfish skin show anti-inflammatory and antifibrotic properties.
- The protective role of CP against cholestatic liver fibrosis is not well understood.
Purpose of the Study:
- To investigate the therapeutic effects of CP on cholestatic liver fibrosis.
- To elucidate the molecular mechanisms underlying CP's action.
- To assess CP's impact on gut microbiota.
Main Methods:
- A bile duct ligation (BDL) mouse model was used to induce cholestatic liver fibrosis.
- CP treatment effects on liver fibrosis, inflammation, oxidative stress, and apoptosis were evaluated.
- Proteomics identified CP targets and signaling pathways.
- 16S rRNA sequencing analyzed gut microbiota diversity.
Main Results:
- CP treatment significantly alleviated bile stasis, liver inflammation, oxidative stress, hepatocyte apoptosis, and liver fibrosis in BDL mice.
- Proteomic analysis revealed CP targets cell adhesion molecules (CAMs), inhibiting the Wnt/β-catenin signaling pathway.
- 16S rRNA sequencing showed CP restored gut microbiota homeostasis.
Conclusions:
- CP effectively mitigates cholestatic liver fibrosis in a mouse model.
- CP exerts its protective effects by modulating CAMs to inhibit Wnt/β-catenin signaling.
- CP also plays a role in restoring gut microbiota homeostasis, contributing to its antifibrotic action.
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