Related Experiment Video
Updated: Sep 25, 2025
Establishment of Hepatocarcinoma in BALB/c-nu Mice and Investigation of the Therapeutic Effect of the Sanleng Jiashen Formula
Published on: January 26, 2024
Ginsenoside Rh2 attenuates CDAHFD-induced liver fibrosis in mice by improving intestinal microbial composition and
Background:
Nowadays, liver diseases are threatening more and more people all over the world and one of the main causes is liver fibrosis. However, there is no effective way to reverse liver fibrosis.
Purpose:
To investigate whether ginsenoside Rh2 (G-Rh2) can alleviate liver fibrosis and elucidate its underlying mechanism.
Methods:
In vivo and in vitro methods were adopted in this research. Choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) was used to feed mice to induce liver fibrosis, and HSC-T6 cells were used to establish an LPS-induced model of liver fibrosis. Through histopathological staining, hematoxylin-eosin (H&E) staining, western blot analysis, intestinal bacteria 16SrRNA sequencing, and other technical means, the research explored whether G-Rh2 possesses anti-fibrotic activity.
Results:
G-Rh2 could notably alleviate CDAHFD-induced liver fibrosis in mice. In particular, it could alleviate liver injury and reduce plasma lipopolysaccharide (LPS) levels. Additionally, G-Rh2 could repair intestinal injury as well as regulate intestinal microbial diversity and composition. HSC-T6 cells could be activated and autophagy could be induced further by LPS in vitro. After being treated with G-Rh2, autophagy was restrained and activation of hepatic stellate cells (HSCs) was controlled. Deeper research showed that G-Rh2 restrained the activation of HSCs via stimulating the AKT-mTOR signaling pathway, restraining autophagy.
Conclusion:
The results of our studies clearly suggest that G-Rh2 repairs intestinal injury, improves intestinal microbial composition, reduces plasma LPS levels, and activates the AKT-mTOR signaling pathway to restrain LPS-mediated autophagy, thus playing an important role in anti-hepatic fibrosis. G-Rh2 was found to have the potential to effectively alleviate liver fibrosis.
Insights
Ginsenoside Rh2 (G-Rh2) alleviates liver fibrosis by repairing gut health and modulating the AKT-mTOR pathway. This natural compound shows potential for reversing liver damage and improving microbial balance.
Area of Science:
- Hepatology
- Pharmacology
- Microbiome research
Background:
- Liver fibrosis is a progressive condition with limited treatment options.
- Effective therapeutic strategies for reversing liver fibrosis are urgently needed.
Purpose of the Study:
- To investigate the anti-fibrotic effects of ginsenoside Rh2 (G-Rh2).
- To elucidate the underlying mechanisms of G-Rh2 in mitigating liver fibrosis.
Main Methods:
- In vivo studies using a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) model in mice.
- In vitro studies using lipopolysaccharide (LPS)-induced hepatic stellate cell (HSC-T6) activation.
- Assessed liver injury, plasma LPS, intestinal integrity, microbial composition, and AKT-mTOR signaling pathway activation.
Main Results:
- G-Rh2 significantly alleviated liver fibrosis and injury in mice, reducing plasma LPS levels.
- G-Rh2 repaired intestinal damage and positively regulated gut microbial diversity and composition.
- G-Rh2 inhibited LPS-induced HSC activation and autophagy by modulating the AKT-mTOR signaling pathway.
Conclusions:
- Ginsenoside Rh2 demonstrates significant potential in treating liver fibrosis.
- G-Rh2 exerts its anti-fibrotic effects by improving gut health, reducing LPS, and inhibiting HSC activation via the AKT-mTOR pathway.
