Psoriasis is a kind of severe immune-mediated systemic skin disorder, becoming a worldwide public health concern. Daturataturin A (DTA), a withanolide compound, exerts excellent anti-inflammatory and anti-proliferative properties. The objective of this study is to elucidate the effect of DTA on psoriasis and its potential mechanism. We established psoriasis-like keratinocytes model by stimulating HaCaT cells with M5 cocktail cytokines including Interleukin (IL)-17A, IL-22, oncostatin M, IL-1α, and tumor necrosis factor-α (TNF-α), followed by intervention with DTA. The potential effects and mechanisms of DTA on psoriasis were evaluated in vitro. DTA was found to be able to inhibit hyperproliferation, promote apoptosis, decrease the release of pro-inflammatory cytokines, downregulate keratin expression, and improve lipid metabolism via regulating the peroxisome proliferator-activated receptor (PPAR) signaling pathway by M5 cocktail cytokines stimulation in HaCaT cells. DTA ameliorated lipid metabolism of psoriasis and exerted the potential anti-psoriasis effects by regulating PPAR pathway in vitro, suggesting that DTA may act as a new therapeutic agent for psoriasis.

银屑病是一种严重的免疫介导的系统性皮肤病，已成为全球公共卫生问题。Daturataturin A （DTA） 是一种醉醺内酯化合物，具有优异的抗炎和抗增殖特性。本研究的目的是阐明 DTA 对银屑病的影响及其潜在机制。我们通过用白细胞介素 （IL） -17A、IL-22、抑瘤素 M、IL-1α 和肿瘤坏死因子-α （TNF-α） 等 M5 鸡尾酒细胞刺激 HaCaT 细胞建立银屑病样角质形成细胞模型，然后用 DTA 干预。在体外评估 DTA 对银屑病的潜在影响和机制。发现 DTA 能够抑制高增殖、促进细胞凋亡、减少促炎细胞因子的释放、下调角蛋白表达，并通过 M5 鸡尾酒细胞因子刺激 HaCaT 细胞来调节过氧化物酶体增殖物激活受体 （PPAR） 信号通路，从而改善脂质代谢。DTA 改善银屑病的脂质代谢，并通过体外调节 PPAR 通路发挥潜在的抗银屑病作用，表明 DTA 可能作为银屑病的新治疗剂。