ArticleBiochemistry and biophysics reports2025
Paridis Rhizoma Saponins ameliorate CCl4-induced liver fibrosis via modulation of the Nrf2-HO-1/NQO-1 and TGF-β1/Smads signaling pathways.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Hepatocyte SLC31A1-dependent copper accumulation contributes to hepatic glucose and lipid metabolic disturbances through AMPKα1 inactivation.Biochemistry and biophysics reports · 2026Article
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7 authors.
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Abstract
Objective/background: Paridis Rhizoma is a common traditional Chinese medicine (TCM), possessing therapeutic effects including heat-clearing, detoxification, and liver calming effects. It is frequently applied in TCM prescriptions for the treatment of liver disease. Studies have shown that total saponins derived from Paridis Rhizoma (PRS) have potent anti-liver fibrosis effect, but its mechanism in treating liver fibrosis has not been clarified. This study aimed to explore the therapeutic effect of PRS on liver fibrosis and elucidate their potential underlying pharmacological mechanisms. Methods: The targets and pathways of Paridis Rhizoma Saponins on experimental liver fibrosis were analyzed using network pharmacology and molecular docking. PRS was administered to rats with CCL Results: Comprehensive network pharmacology and animal experiments show that PRS may act on STAT3, SRC, VEGFA, AKT1 and other targets through its polyphyllin I, polyphyllin II, polyphyllin VI, polyphyllin VII and other components.Analysis from ELISA showed that PRS could improve liver function, mitigate the progression of liver fibrosis, and regulate inflammatory responses in rats. Morphological, H&E, and Masson's staining demonstrated that PRS significantly improved liver tissue immune response and necrosis. Additionally, IHC staining, WB results, and RT-qPCR results showed that PRS positively regulates the Nrf2-HO-1/NQO-1 and TGF-β1/Smads signaling pathways to counteract the development of pathological liver fibrosis in rats. Conclusion: These findings indicate that PRS can mitigate the impact of CCl
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