Objective: As a common chronic inflammatory skin disease, psoriasis seriously affects the physical health and psychological well-being of patients. Various clinical treatments for psoriasis have their own drawbacks, so it is important to find effective and safe drugs. Rehmannioside A (ReA) has anti-inflammatory properties and is the main active ingredient in Fuzhengzhiyanghefuzhiyang decoction (FZHFZY), an herbal compound for the treatment of psoriasis. But no studies have been conducted to determine whether ReA alone can treat psoriasis. Therefore, this study was designed to investigate the effect of ReA in the treatment of psoriasis and its potential mechanism of action.
Methods: HaCaT cells were treated with ReA and IL-17A alone for 24 h and 48 h, and the most effective concentrations of ReA and interleukin (IL)-17A were found at 25 μg/mL and 100 ng/mL, respectively. A psoriasis cell model was constructed by stimulating HaCaT cells with IL-17A, followed by intervention with ReA. Cell viability and cell cycle distribution were measured by MTT assay and flow cytometry. The expression levels of keratin family members and chemokines were detected by real-time quantitative PCR (RT-qPCR), the levels of pro-inflammatory cytokines by enzyme-linked immunosorbent assay (ELISA), and key proteins of TRAF6/MAPK signaling pathway by Western blot.
Results: ReA weaken cell viability, down-regulate the expression of keratin family members (KRT6 and KRT17), restore cell cycle distribution to normal distribution, inhibit the release of pro-inflammatory cytokines (IL-6, IL-8 and IL-1β) and lower the expression of chemokines (S100A7, S100A9 and CXCL2) by interfering with the interaction between HaCaT cells and IL-17A. Thus, it exerts an anti-psoriatic effect by reducing the inflammatory response and inhibiting abnormal proliferation of HaCaT cells. Mechanistically, ReA inhibited the TRAF6/MAPK signaling pathway activated by IL-17A stimulation in HaCaT cells.
Conclusion: ReA has in vitro anti-psoriatic effects and may be a new therapeutic agent for psoriasis.

Keywords: psoriasis, rehmannioside A, ReA, interleukin-17A, IL-17A, inflammation, proliferation


中文翻译：

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地黄苷 A 通过干扰 HaCaT 细胞与 IL-17A 的相互作用来抑制 TRAF6/MAPK 通路并改善银屑病

目的：银屑病作为一种常见的慢性炎症性皮肤病，严重影响患者的身体健康和心理健康。临床上治疗银屑病的各种治疗方法都有各自的缺点，因此寻找有效、安全的药物非常重要。地黄苷 A (ReA) 具有抗炎特性，是扶正止痒和扶止痒汤 (FZHFZY) 的主要活性成分，这是一种治疗牛皮癣的草药复方。但尚未进行任何研究来确定 ReA 是否可以单独治疗牛皮癣。因此，本研究旨在探讨ReA治疗银屑病的效果及其潜在作用机制。
方法： HaCaT 细胞单独用 ReA 和 IL-17A 处理 24 h 和 48 h，ReA 和白细胞介素 (IL)-17A 的最有效浓度分别为 25 μg/mL 和 100 ng/mL。通过用 IL-17A 刺激 HaCaT 细胞，然后用 ReA 干预，构建银屑病细胞模型。通过MTT测定和流式细胞术测量细胞活力和细胞周期分布。采用实时定量PCR（RT-qPCR）检测角蛋白家族成员和趋化因子的表达水平，采用酶联免疫吸附试验（ELISA）检测促炎细胞因子的水平，采用TRAF6/MAPK信号通路关键蛋白的表达水平。蛋白质印迹。
结果： ReA削弱细胞活力，下调角蛋白家族成员（KRT6和KRT17）的表达，使细胞周期分布恢复正常分布，抑制促炎细胞因子（IL-6、IL-8和IL-1β）的释放）并通过干扰 HaCaT 细胞与 IL-17A 之间的相互作用来降低趋化因子（S100A7、S100A9 和 CXCL2）的表达。因此，它通过减少炎症反应和抑制 HaCaT 细胞的异常增殖来发挥抗银屑病作用。从机制上讲，ReA 抑制 HaCaT 细胞中由 IL-17A 刺激激活的 TRAF6/MAPK 信号通路。
结论： ReA具有体外抗银屑病作用，可能成为银屑病的新治疗药物。

关键词：银屑病，生地黄苷 A，ReA，白细胞介素 17A，IL-17A，炎症，增殖