Tanshinone IIA attenuates psoriasis via Nrf2/HO-1 activation: Mechanistic insights from preclinical models.

BACKGROUND

Psoriasis is a chronic inflammatory skin disorder driven by oxidative stress and immune dysregulation. Tanshinone IIA, a bioactive compound from Salvia miltiorrhiza, exhibits antioxidant properties, but its role in treating psoriasis remains underexplored.

METHODS

Using H2O2-stimulated HaCaT keratinocytes and an imiquimod (IMQ)-induced murine psoriasis model, we investigated the therapeutic effects of tanshinone IIA. Key assays included Reactive Oxygen Species (ROS) detection, EdU/CCK8 proliferation analysis, real-time quantitative PCR (RT-qPCR), western blotting, and immunohistochemistry to evaluate nuclear factor erythroid 2-related factor 2 (Nrf2) activation, antioxidant protein expression, and histopathological changes.

RESULTS

Tanshinone IIA significantly suppressed TNF-α-induced HaCaT proliferation and ROS accumulation. Mechanistically, it promoted Nrf2 nuclear translocation and upregulated HO-1, SOD2, and NQO1 expression. In IMQ-treated mice, it reduced epidermal thickness, scaling, and inflammatory cytokines while enhancing antioxidant defences.

CONCLUSION

Tanshinone IIA mitigates psoriasis via Nrf2/HO-1 activation and thus has therapeutic potential.