ArticleActa pharmacologica Sinica2025
Luteolin-7-diglucuronide, a novel PTP1B inhibitor, ameliorates hepatic stellate cell activation and liver fibrosis in mice.
Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- From diet to disease modulation: the multi-targeted effects of medicinal-food homologous plants in hepatic fibrosis.Frontiers in nutrition · 2026Review
- Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer.Frontiers in pharmacology · 2026Review
- LGALS3 promotes liver fibrosis by enhancing the expression and phosphorylation of ERK1/2.European journal of medical research · 2025Article
- Inhibition of PGK1 ameliorates acute kidney injury through inactivating the PKM2/ALOX12/ferroptosis pathway in a study with male mice.Nature communications · 2025Article
- Mechanistic insights into post-translational modifications in hepatic fibrosis: pathogenic roles and therapeutic potentials.Journal of translational medicine · 2025Review
- Investigation of Bioactive Compounds Extracted fromPharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring hepatic stellate cell-driven fibrosis: therapeutic advances and future perspectives.ADMET & DMPK · 2025Review
- Natural medicines for treating liver fibrosis by modulating post-translational modifications.Frontiers in pharmacology · 2025Review
- Non-parenchymal cells: key targets for modulating chronic liver diseases.Frontiers in immunology · 2025Review
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11 authors.
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Abstract
Liver fibrosis, one of the leading causes of morbidity and mortality worldwide, lacks effective therapy. The activation of hepatic stellate cells (HSCs) is the dominant event in hepatic fibrogenesis. Luteolin-7-diglucuronide (L7DG) is the major flavonoid extracted from Perilla frutescens and Verbena officinalis. Their beneficial effects in the treatment of liver diseases were well documented. In this study we investigated the anti-fibrotic activities of L7DG and the potential mechanisms. We established TGF-β1-activated mouse primary hepatic stellate cells (pHSCs) and human HSC line LX-2 as in vitro liver fibrosis models. Co-treatment with L7DG (5, 20, 50 μM) dose-dependently decreased TGF-β1-induced expression of fibrotic markers collagen 1, α-SMA and fibronectin. In liver fibrosis mouse models induced by CCl
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