Department of Dermatology, Hainan Hospital of Traditional Chinese Medicine, Haikou, China.
Department of Oncology, Hainan Hospital of Traditional Chinese Medicine, Haikou, China.
Skin Res Technol. 2024 Feb;30(2):e13577. doi: 10.1111/srt.13577.
Psoriasis is a persistent inflammatory dermatological disorder. Tanshinone IIA (tan-IIA) is a biologically active compound in the self-made Xiao-Yin decoction (SMXYD) and exhibits diverse biological properties, such as anti-proliferative and anti-inflammatory effects. The objective of this investigation was to assess the potential of tan-IIA as a therapeutic agent against psoriasis.
Network pharmacology was employed to ascertain the active constituents and potential pathways associated with SMXYD and psoriasis. We conducted CCK-8, qRT-PCR, and western blotting to assess the proliferation of HaCaT keratinocytes and the expression of IL-17/IL-23 and PTGS2/NF-κB/AP-1 pathways. Additionally, we used H&E staining, western blotting, and ELISA to evaluate the therapeutic effects and signaling pathways of tan-IIA in psoriasis-like mice induced by imiquimod (IMQ).
Network pharmacology analysis identified eight hub compounds. The Th17/IL-17 signaling was found to be a potential therapeutic pathway of SMXYD against psoriasis, with JUN (AP-1) as the core molecule. Next, PTGS2 was selected as the target of tan-IIA against psoriasis using network pharmacology analysis. Molecular docking showed a high affinity between PTGS2 and tan-IIA. Tan-IIA treatment attenuated M-5-induced hyperproliferation and inflammation in HaCaT keratinocytes. Additionally, Tan-IIA downregulated the PTGS2/NF-κB/AP-1 pathway in HaCaT keratinocytes. In the IMQ-induced psoriasis-like mouse, tan-IIA significantly reduced the severity of skin lesions and downregulated the PTGS2/NF-κB/AP-1 pathway. Moreover, the combination of methotrexate (MTX) and tan-IIA further inhibited the IL-17/IL-23 and PTGS2/NF-κB/AP-1 pathways.
The administration of tan-IIA has shown a positive effect on psoriasis by inhibiting the IL-17/IL-23 and PTGS2/NF-κB/AP-1 pathways. The findings suggest that it has promising qualities that make it a potential candidate for the development of future anti-psoriatic agents.
银屑病是一种持续性炎症性皮肤病。丹参酮 IIA（tan-IIA）是自拟消银方（SMXYD）中的一种具有生物活性的化合物，具有多种生物特性，如抗增殖和抗炎作用。本研究旨在评估 tan-IIA 作为治疗银屑病的潜在药物。
采用网络药理学方法确定 SMXYD 及银屑病相关的活性成分及潜在途径。我们通过 CCK-8、qRT-PCR 和 Western blot 检测 HaCaT 角质形成细胞的增殖以及 IL-17/IL-23 和 PTGS2/NF-κB/AP-1 途径的表达。此外，我们使用 H&E 染色、Western blot 和 ELISA 评估了角叉菜胶诱导的银屑病样小鼠中 tan-IIA 的治疗作用和信号通路。
网络药理学分析鉴定出 8 个枢纽化合物。Th17/IL-17 信号通路被认为是 SMXYD 治疗银屑病的潜在途径，其中 JUN（AP-1）是核心分子。接下来，我们使用网络药理学分析选择 PTGS2 作为 tan-IIA 治疗银屑病的靶点。分子对接表明 PTGS2 与 tan-IIA 具有高亲和力。Tan-IIA 治疗可减轻 M-5 诱导的 HaCaT 角质形成细胞过度增殖和炎症。此外，Tan-IIA 下调了 HaCaT 角质形成细胞中的 PTGS2/NF-κB/AP-1 通路。在咪喹莫特（IMQ）诱导的银屑病样小鼠中，tan-IIA 显著减轻皮肤病变的严重程度，并下调了 PTGS2/NF-κB/AP-1 通路。此外，甲氨蝶呤（MTX）与 tan-IIA 联合使用进一步抑制了 IL-17/IL-23 和 PTGS2/NF-κB/AP-1 通路。
Tan-IIA 通过抑制 IL-17/IL-23 和 PTGS2/NF-κB/AP-1 通路对银屑病有积极作用。研究结果表明，它具有开发未来抗银屑病药物的潜在候选药物的良好品质。
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