ArticleFrontiers in veterinary science2025
Arbutin protects against methotrexate-induced pulmonary injury in rats via modulation of oxidative stress, inflammation, and ER stress.
Article in Frontiers in veterinary science, 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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3 citing papers in PubMed.
- Current perspectives on natural and pharmacological interventions for combating drug-induced pulmonary toxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- L-Methionine attenuates methotrexate-induced cardiotoxicity by modulating oxidative stress, inflammation, and dyslipidemia in rats.Toxicology reports · 2026Article
- Ameliorative Role of Silymarin in Methotrexate-Induced Pulmonary Damage: A Multi-Pathway Molecular Approach.Journal of biochemical and molecular toxicology · 2026Article
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7 authors.
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Abstract
Introduction: Methotrexate (MTX) is a widely utilized agent in the treatment of cancer, yet it is notable that it can induce pulmonary toxicity in cases of high-dose chemotherapy. Arbutin (ARB) is a hydroquinone compound that is present in members of the Lamiaceae, Ericaceae and Rosaceae families, and experimental studies have demonstrated its capacity for lung protection. The present study aimed to determine whether ARB could reduce the pulmonary toxicity of MTX and to explore the underlying mechanisms. Methods: The lung toxicity rat model was created by means of a single intraperitoneal injection of MTX at a dose of 20 mg/kg. The animals were then treated with two different doses of ARB (50 and 100 mg/kg) for a period of 7 days. Following the conclusion of the treatment period, a histopathological examination of the lung tissue samples was conducted. The remaining tissue samples were evaluated for oxidative stress (OS), inflammation, endoplasmic reticulum stress (ERS), sirtuin 1 (SIRT1)/nuclear factor erythroid-related factor 2 (Nrf2) pathway, and apoptosis for further analysis. Results: The administration of MTX resulted in the inhibition of SIRT1/Nrf2 in lung tissue, accompanied by an escalation in OS, inflammation, ERS, and apoptosis levels. This was concomitant with a significant enhancement in the severity of histopathological findings. Nevertheless, ARB reversed MTX-induced biochemical and pathological changes through SIRT1/Nrf2 modulation. Discussion: It is asserted that further comprehensive studies are required to support the hypothesis that ARB has the potential to improve oxidative and inflammatory lung injury via SIRT1/Nrf2 modulation.
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