ArticleJournal of ginseng research2025
Notoginsenoside R2 attenuates hepatic fibrosis via STAT3-dependent hepatic stellate cells senescence induction and inflammatory microenvironment suppression.
Article in Journal of ginseng research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Ginsenosides Rh2 and Rg3 in first-line combination therapy: Prospects for rapid clinical translation in drug-resistant triple-negative breast cancer.Journal of ginseng research · 2026Review
- Korean red ginseng saponins ameliorate metabolic dysfunction-associated steatohepatitis in mice by inhibiting caspase-11 and NLRP3 inflammasomes.Journal of ginseng research · 2026Article
- Ginsenosides fromJournal of ginseng research · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatic fibrosis (HF) continues to be a significant global health concern, substantially contributing to morbidity and mortality due to the absence of effective therapeutic options. This study examines the pharmacological effectiveness and underlying mechanisms of Notoginsenoside R2 (R2) in mitigating HF, aiming to find a new multifunctional candidate for therapeutic application. Methods: An integrative methodology utilizing network pharmacology, molecular docking, and experimental validation was implemented. Results: Network pharmacology identified 32 common targets between R2 and HF, with a particular emphasis on pathways critical for the activation of HSCs. Molecular docking confirmed strong interactions between R2 and signal transducer and activator of STAT3. Conclusion: This study identified R2 as a regulator of STAT3 with dual antifibrotic effects: reduction of the inflammatory microenvironment and induction of senescence. These findings position R2 as a viable treatment candidate for HF, necessitating additional clinical investigation.
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Registered trials
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