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

Abstract

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.

Key Findings

• Tanshinone IIA significantly suppressed TNF-α-induced HaCaT keratinocyte proliferation and ROS accumulation.
• Tanshinone IIA promoted Nrf2 nuclear translocation and upregulated antioxidant proteins HO-1, SOD2, and NQO1.
• In an imiquimod-induced murine psoriasis model, tanshinone IIA reduced epidermal thickness, scaling, inflammatory cytokines, and enhanced antioxidant defenses.

Clinical Significance

Citation

Xu Xia, Liang Jingyao, Huang Maofanget al.. Tanshinone IIA attenuates psoriasis via Nrf2/HO-1 activation: Mechanistic insights from preclinical models. Biochemistry and biophysics reports. 2026-Jun.