Psoriasis is a chronic inflammatory skin disease characterized by hyperproliferation of keratinocytes and a pro-inflammatory milieu in the skin. While patients with moderate to severe psoriasis are treated using targeted therapies (small molecules and monoclonal antibodies), patients suffering from milder forms are still in need of effective topical products without adverse effects. Antimony compounds (ACs) are regularly used as anti-inflammatory compounds in traditional and anthroposophic medicine and as antiprotozoan drugs. Here, we examined the effect of metallic antimony, natural antimony(III) sulfide and potassium antimonyl(III) tartrate in vitro on psoriasis-like keratinocytes and the human dendritic cell line THP-1 using qPCR, immunocytochemistry, ELISA and flow cytometry. In psoriatic keratinocytes, ACs inhibited the overexpression of the antimicrobial peptide β-defensin 2 and glucose transporter 1, as well as the hyperproliferation marker keratin 17. Furthermore, ACs mediated anti-inflammatory effects by reducing nuclear translocation of the p65 subunit of NF-κB and pSTAT3 and inhibited pro-inflammatory cytokine secretion by keratinocytes. In addition, ACs displayed anti-psoriatic effects by reducing the activation of IFN-α-treated THP-1 cells as well as the expression of the psoriasis-promoting master cytokine IL-23 by these cells. While all ACs showed anti-psoriatic effects, the most prominent results were seen with potassium antimonyl(III) tartrate. In summary, ACs display numerous anti-psoriatic effects in vitro at subtoxic concentrations. We conclude that ACs are interesting compounds for the topical treatment of psoriasis that warrant further investigation in clinical studies.

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锑化合物在体外的抗银屑病作用

银屑病是一种慢性炎症性皮肤病，其特征是角质细胞过度增殖和皮肤中的促炎环境。虽然使用靶向疗法（小分子和单克隆抗体）治疗中度至重度银屑病患者，但轻度银屑病患者仍需要有效且无副作用的局部产品。锑化合物 (AC) 经常用作传统和人智医学中的抗炎化合物以及抗原虫药物。在这里，我们使用 qPCR、免疫细胞化学、ELISA 和流式细胞术检测了金属锑、天然硫化锑 (III) 和酒石酸锑 (III) 钾对银屑病样角质形成细胞和人树突状细胞系 THP-1 的影响。在银屑病角质形成细胞中，ACs 抑制了抗菌肽 β-防御素 2 和葡萄糖转运蛋白 1 以及过度增殖标志物角蛋白 17 的过度表达。 此外，ACs 通过减少 NF-κB 和 pSTAT3 的 p65 亚基的核易位来介导抗炎作用，并抑制角质形成细胞分泌促炎细胞因子。此外，ACs 通过减少 IFN-α 处理的 THP-1 细胞的活化以及这些细胞对促进银屑病的主细胞因子 IL-23 的表达，显示出抗银屑病作用。虽然所有 AC 均显示出抗银屑病作用，但最显着的结果是酒石酸锑 (III) 钾。总之，ACs 在体外在亚毒性浓度下显示出多种抗银屑病作用。