# Vincamine Mitigates Methotrexate-Induced Liver Fibrosis Model

**Authors:** Yonca Yılmaz Ürün, Gürkan Güner, Ejder Saylav Bora, Ayşe Buket Taşkın, Muslih Ürün, Oytun Erbaş

PMC · DOI: 10.5152/tjg.2025.24716 · The Turkish Journal of Gastroenterology · 2025-06-23

## TL;DR

This study shows that vincamine helps reduce liver damage caused by methotrexate in rats by acting as an antioxidant, anti-inflammatory, and anti-fibrotic agent.

## Contribution

The study demonstrates vincamine's novel therapeutic potential in mitigating methotrexate-induced liver fibrosis in rats.

## Key findings

- Vincamine significantly reduced plasma and liver markers of oxidative stress and inflammation.
- Histopathological analysis confirmed that vincamine protected against liver injury.
- Vincamine improved liver function both biochemically and structurally.

## Abstract

Liver fibrosis is linked to higher rates of death and disease. This study examined the hepatoprotective properties of vincamine and its potential therapeutic application in treating liver damage caused by methotrexate in rats.

Thirty male Wistar albino rats, with weights ranging from 150 to 200 g and ages between 10 and 12 weeks, were included in the study. A total of 10 rats were selected to serve as the control group, receiving no medication. A group of 20 rats was given a single intraperitoneal dose of 20 mg/kg methotrexate in order to cause liver damage. Subsequently, the participants were randomly allocated into 2 cohorts and administered either 1 mL/kg/day tap water or 50 mg/kg/day vincamine orally through gavage on a daily basis for a duration of 10 days. Following the completion of the treatment period, the animals were euthanized and their livers were examined histologically. Furthermore, the levels of plasma galectin-3 (gal-3), cytokeratin 18, malondialdehyde (MDA), alanine transaminase (ALT), liver MDA, and transforming growth factor beta (TGF-β) levels were evaluated. Results: Treatment with vincamine resulted in a significant decrease in plasma gal-3, cytokeratin, MDA, and ALT levels and liver MDA and TGF-β levels compared to the methotrexate and saline group. Vincamine treatment effectively protected against liver injury, and histopathological examination of the livers confirmed these results. Conclusion: This study demonstrates that vincamine alleviates methotrexate-induced liver toxicity via exhibiting antioxidant, anti-inflammatory, and anti-fibrotic activities and improved liver functionally, biochemically, and histopathologically.

## Linked entities

- **Proteins:** LGALS3 (galectin 3), TGFB1 (transforming growth factor beta 1)
- **Chemicals:** vincamine (PubChem CID 15376), methotrexate (PubChem CID 4112), malondialdehyde (PubChem CID 10964)

## Full-text entities

- **Genes:** Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 59086] {aka Tgfb}, Krt18 (keratin 18) [NCBI Gene 294853] {aka Krt1-18}, Lgals3 (galectin 3) [NCBI Gene 83781] {aka AGE-R3, CBP30, L-34, gal-3}
- **Diseases:** liver injury (MESH:D017093), Liver Fibrosis (MESH:D008103), death (MESH:D003643), liver damage (MESH:D056486)
- **Chemicals:** Vincamine (MESH:D014749), MDA (MESH:D008315), Methotrexate (MESH:D008727)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12520132/full.md

## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12520132/full.md

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Source: https://tomesphere.com/paper/PMC12520132