ArticleJournal of biochemical and molecular toxicology2026
Ameliorative Role of Silymarin in Methotrexate-Induced Pulmonary Damage: A Multi-Pathway Molecular Approach.
Article in Journal of biochemical and molecular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Research Progress and Prospects of Flavonoids in the Treatment of Diseases by Regulating Autophagy: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
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3 authors.
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Abstract
Methotrexate (MTX) is a medication that is frequently prescribed for the treatment of both malignant disorders and inflammatory pathologies. However, its use is limited by dose-dependent pulmonary toxicity. The present study investigated the protective effects of silymarin (SLM) against MTX-induced lung injury by evaluating apoptosis, oxidative stress, autophagy, inflammation and histopathological changes in rats. Twenty-eight Wistar albino rats were assigned to the Control, SLM (50 mg/kg, p. o.), MTX (20 mg/kg, i. p.), and MTX + SLM groups. MTX treatment led to a significant elevation in malondialdehyde levels along with marked reductions in glutathione content and antioxidant enzyme activities, concomitant with decreased Nrf2 and HO-1 expression, indicating pronounced oxidative stress (p < 0.05). Additionally, MTX has been shown to raise Bax and Caspase-3 and diminish Bcl-2 while simultaneously inducing NF-κB, TNF-α, TLR-4, and HMGB1. This confirms the presence of increased inflammation and mitochondrial-dependent apoptosis (p < 0.05). Furthermore, MTX elevated the expression of LC3A, LC3B, and Beclin-1, suggesting an increase in autophagy (p < 0.05). SLM supplementation greatly improved antioxidant status, increased Nrf2/HO-1, decreased inflammatory signaling, modulated Caspase-3/Bax/Bcl-2 expression, and suppressed MTX-induced autophagy (p < 0.05). These biochemical findings were subsequently corroborated by histopathological analysis. In summary, the present study demonstrates that SLM offers a promising protective effect against MTX-induced pulmonary damage, operating through mechanisms involving antioxidant, anti-autophagic, anti-inflammatory and anti-apoptotic actions. These results underscore the potential of SLM as a complementary therapeutic agent in mitigating lung toxicity induced by chemotherapy agents.
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