Tanshinone IIA attenuates psoriasis via Nrf2/HO-1 activation: Mechanistic insights from preclinical models
- Biochem Biophys Rep. 2026 May 11:46:102606. doi: 10.1016/j.bbrep.2026.102606.
- 1. Department of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
- 2. Department of Clinical Laboratory, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, China.
- 3. Department of Pharmacy, The Seventh Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
- 4. Department of Dermatology, Panyu Maternal and Child Care Service Centre of Guangzhou, Guangzhou, Guangdong, China.
- 5. Department of Clinical Laboratory, Eighth Affiliated Hospital of Guangxi Medical University, Guigang City People's Hospital, Guigang, Guangxi, China.
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.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: VEGFR