Evidence map›Paper›PMID 38774203›Full record

ArticleClinical and experimental hepatology2023

Methotrexate-induced hepatotoxicity in rats and the therapeutic properties of vitamin E: a histopathologic and flowcytometric research.

Ahmet U Akman, Zuleyha Erisgin, Sibel Turedi, Yavuz Tekelioglu

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Article in Clinical and experimental hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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5 citing papers in PubMed.

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5 · Who and what money

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4 authors.

Ahmet U AkmanDepartment of Histology and Embryology, Faculty of Medicine, Amasya University, Turkey.
Zuleyha ErisginDepartment of Histology and Embryology, Faculty of Medicine, Giresun University, Turkey.
Sibel TurediDepartment of Histology and Embryology, Faculty of Medicine, Harran University, Turkey.
Yavuz TekeliogluDepartment of Histology and Embryology, Faculty of Medicine, Karadeniz Technical University, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aim of the study: Methotrexate (MTX) causes oxidative stress-related liver damage. Our objective was to investigate the protective effects of vitamin E against MTX-induced hepatotoxicity through histopathological methods and flow cytometry. Material and methods: The rats were assigned to four groups: Control (2 ml saline for 5 days), MTX (20 mg/kg intraperitoneally (i.p.) only on the initial day of the study), MTX + vitamin E (20 mg/kg MTX (i.p.) only on the first day, and 100 mg/kg vitamin E (i.p.) was applied for 5 days during the study), Vitamin E (100 mg/kg of vitamin E (i.p.) was given for five days). Histopathologic changes and the flow cytometric apoptotic index were evaluated for liver tissue. The Kruskal-Wallis test was used for comparisons between groups. The statistical significance level was accepted as Results: In the histopathological analysis, hepatocyte degeneration, dilatation of sinusoids, mononuclear cell infiltration, hydropic degeneration in hepatocytes, vacuolization, and pycnotic nucleus were observed in the MTX group. In the MTX + vitamin E group, hepatocyte degeneration, pycnotic nuclei, and dilatation in sinusoids were significantly lower compared to the MTX group. In the MTX group, glycogen accumulation in hepatocytes was lower compared to the control group. In the MTX + vitamin E group, glycogen accumulation in hepatocy-tes was higher compared to the MTX group. The flowcytometric apoptotic index (AI) percentage in the MTX group was 34.4% and in the MTX + vitamin E group the value was 9.4%. Conclusions: Our results demonstrated that vitamin E ameliorates MTX-induced liver damage. Co-using vitamin E and MTX drugs will be beneficial for the treatment of various diseases.

Indexed as

flow cytometrylivermethotrexateratsvitamin E

Identifiers

PMID38774203
PMCPMC11103801

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