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.

牛皮癣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) 是一种茄内酯化合物，具有优异的抗炎和抗增殖特性。本研究的目的是阐明DTA对银屑病的作用及其潜在机制。我们通过用M5鸡尾酒细胞因子（包括白细胞介素（IL）-17A、IL-22、制瘤素M、IL-1α和肿瘤坏死因子-α（TNF-α））刺激HaCaT细胞，建立银屑病样角质形成细胞模型，然后进行干预差热分析。体外评估了 DTA 对银屑病的潜在作用和机制。研究发现，DTA 通过 M5 鸡尾酒细胞因子刺激调节过氧化物酶体增殖物激活受体 (PPAR) 信号通路，能够抑制 HaCaT 中的过度增殖、促进细胞凋亡、减少促炎细胞因子的释放、下调角蛋白表达并改善脂质代谢。细胞。 DTA改善银屑病脂质代谢，在体外通过调节PPAR通路发挥潜在的抗银屑病作用，提示DTA可能作为银屑病的新治疗药物。