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Background: Silibinin has shown therapeutic effects in various inflammatory and cancer models. However, the therapeutic effect and underlying mechanism in V2O5-induced pulmonary inflammation, which consists of particulate matter and metal components, have not been identified. We examined the potential anti-inflammatory activity and underlying mechanism of silibinin in a vanadium-induced lung injury model.

Results: Silibinin treatment resulted in a significant restoration of cell viability and reduced infiltration of inflammatory cells in a histological analysis. In addition, silibinin significantly reduced the expression of the pro-inflammatory cytokines, TNF-α, IL-6, and IL-1ꞵ. Furthermore, silibinin reduced inflammation by down-regulating the MAPK and NF-kB signaling pathways and the NLRP3 inflammasome. Treatment with silibinin significantly reduced the NLRP3 expression levels in lung tissue.

Conclusion: These results indicate that silibinin exhibits anti-inflammatory effects in V2O5-induced inflammatory mice.