■作为一种常见的慢性炎症性皮肤病,银屑病严重影响患者的身体健康和心理健康。牛皮癣的各种临床治疗方法都有其自身的缺点,所以找到有效和安全的药物很重要。地黄苷A(ReA)具有抗炎特性,是扶正止炎止咳止痒汤(FZHFZY)的主要活性成分,一种治疗牛皮癣的草药化合物。但尚未进行任何研究来确定单独使用ReA是否可以治疗牛皮癣。因此,本研究旨在探讨ReA在银屑病治疗中的作用及其潜在作用机制。
■HaCaT细胞用ReA和IL-17A单独处理24小时和48小时,发现ReA和白细胞介素(IL)-17A的最有效浓度为25μg/mL和100ng/mL,分别。通过用IL-17A刺激HaCaT细胞构建银屑病细胞模型,随后是ReA的干预。通过MTT法和流式细胞术测量细胞活力和细胞周期分布。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,酶联免疫吸附试验(ELISA)检测促炎细胞因子水平,和TRAF6/MAPK信号通路关键蛋白的Westernblot。
■ReA削弱细胞活力,下调角蛋白家族成员(KRT6和KRT17)的表达,恢复细胞周期分布到正态分布,通过干扰HaCaT细胞与IL-17A之间的相互作用,抑制促炎细胞因子(IL-6,IL-8和IL-1β)的释放并降低趋化因子(S100A7,S100A9和CXCL2)的表达。因此,它通过减少炎症反应和抑制HaCaT细胞的异常增殖而发挥抗银屑病作用。机械上,ReA抑制HaCaT细胞中IL-17A刺激激活的TRAF6/MAPK信号通路。
■ReA具有体外抗银屑病作用,可能是一种新的银屑病治疗剂。
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: ReA has in vitro anti-psoriatic effects and may be a new therapeutic agent for psoriasis.