ArticleIn vivo (Athens, Greece)
Silibinin Mitigates Vanadium-induced Lung Injury
Article in In vivo (Athens, Greece). 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.
- Network Pharmacology and Experimental Validation Elucidate the Anti-Angiogenic Mechanism of Silibinin.Chemistry & biodiversity · 2026Article
- Pharmaceutical therapies for pyroptosis in lung injury.Inflammopharmacology · 2026Review
- Silibinin mitigates AKI-to-CKD transition via MAPK and PI3K/AKT signaling pathways in Ischemia-Reperfusion injury.Scientific reports · 2025Article
- Silibinin Suppresses Inflammatory Responses Induced by Exposure to Asian Sand Dust.Antioxidants (Basel, Switzerland) · 2024Article
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13 authors.
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Abstract
BACKGROUND/
aimSilibinin, has been investigated for its potential benefits and mechanisms in addressing vanadium pentoxide (V2O5)-induced pulmonary inflammation. This study explored the anti-inflammatory activity of silibinin and elucidate the mechanisms by which it operates in a mouse model of vanadium-induced lung injury. MATERIALS AND
methodsEight-week-old male BALB/c mice were exposed to V2O5 to induce lung injury. Mice were pretreated with silibinin at doses of 50 mg/kg and 100 mg/kg. Histological analyses were performed to assess cell viability and infiltration of inflammatory cells. The expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and activation of the MAPK and NF-[Formula: see text]B signaling pathways, as well as the NLRP3 inflammasome, were evaluated using real-time PCR, western blot analysis, and immunohistochemistry. Whole blood analysis was conducted to measure white blood cell counts.
resultsSilibinin treatment significantly improved cell viability, reduced inflammatory cell infiltration, and decreased the expression of pro-inflammatory cytokines in V2O5-induced lung injury. It also notably suppressed the activation of the MAPK and NF-[Formula: see text]B signaling pathways, along with a marked reduction in NLRP3 inflammasome expression levels in lung tissues. Additionally, silibinin-treated groups exhibited a significant decrease in white blood cell counts, including neutrophils, lymphocytes, and eosinophils.
conclusionThese findings underscore the potent anti-inflammatory effects of silibinin in mice with V2O5-induced lung inflammation, highlighting its therapeutic potential. The study not only confirms the efficacy of silibinin in mitigating inflammatory responses but also provides a foundational understanding of its role in modulating key inflammatory pathways, paving the way for future therapeutic strategies against pulmonary inflammation induced by environmental pollutants.
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