ArticleMolecular medicine reports2019
Combination leflunomide and methotrexate impedes the recovery of liver fibrosis, partly through inhibition of myeloid cell admittance.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The dual anti-inflammatory and anticoagulant effects of Jianpi Huashi Tongluo prescription on Rheumatoid Arthritis through inhibiting the activation of the PI3K/AKT signaling pathway.Frontiers in pharmacology · 2025Article
- IL-33 Promotes ST2-Dependent Fibroblast Maturation via P38 and TGF-β in a Mouse Model of Epidural Fibrosis.Tissue engineering and regenerative medicine · 2022Article
- Combination therapy of ginsenoside compound K and methotrexate was efficient in elimination of anaemia and reduction of disease activity in adjuvant-induced arthritis rats.Pharmaceutical biology · 2020Article
- Neutrophil extracellular traps promote scar formation in post-epidural fibrosis.NPJ Regenerative medicine · 2020Article
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Authors and funding
5 authors.
Funding
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Abstract
The process of liver fibrosis is reversible and involves a recovery phase. In the present study, the potential side effects of combination leflunomide and methotrexate (LEF+MTX), a conventional rheumatoid arthritis therapy used in the resolution of liver fibrosis, was investigated. In a carbon tetrachloride‑induced liver fibrosis model, the results of hepatic pathology demonstrated that the LEF+MTX combination delayed the recovery of fibrosis, although the activation of hepatic stellate cells in vitro was inhibited. A total of four liver fibrosis‑associated indicators, hyaluronic acid, laminin, procollagen type III and collagen IV, maintained high levels in the serum of LEF+MTX‑treated mice, while detection of bone marrow‑driven monocytes in the blood by flow cytometry indicated that they were significantly decreased. Notably, the results of immunofluorescence staining of hepatic myeloid cells and detection of vascular growth factor A (VEGF‑A) in blood and liver suggested that the reduced degeneration of collagen in liver sinusoids was associated with decreased myeloid cell adhesion and the downregulation of VEGF‑A in the liver. The present results suggested that in certain cases, treatment with LEF+MTX may impede the recovery of hepatic fibrosis‑associated diseases in mice.
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