银屑病被认为是一种以角质形成细胞过度增殖为特征的慢性炎性皮肤病。IL-23/IL-17免疫途径已在许多研究中被证实与银屑病进展密切相关。银屑I配方是由9种草药制成的中药,在银屑病中具有优异的临床疗效。然而,到目前为止,银屑I方抗银屑病的作用机制尚不清楚。从这个角度来看,我们讨论了银屑I方在咪喹莫特(IMQ)诱导的银屑病小鼠中的功效。银屑I组能显著降低银屑病小鼠皮肤损伤面积和炎症反应。此外,银屑Ⅰ号方减轻炎症相关基因IL-6、IL-17A的表达水平,IL-22、IL-23、TNF-α和IL-23、IL-18、IL-6和IL-1β相关蛋白,减轻树突状细胞的异常激增,巨噬细胞和T细胞在皮肤和脾脏。同时我们发现银屑I号降低了NO的释放,TNF-α,脂多糖诱导的小鼠巨噬细胞RAW264.7细胞系中的IL-1β和IL-23。该结果表明,银屑I式的治疗机制也可能与STAT信号通路有关。我们进一步分析了银屑I配方的活性成分,佛陀赛德,这可能是发挥治疗作用的主要物质。总之,我们已经研究了银屑I配方通过抑制IL-23/IL-17轴来减弱银屑病中IMQ诱导的炎症反应,奠定了抗银屑病作用机制的基础,为银屑I方的临床推广提供了理论依据。
Psoriasis is considered a chronic inflammatory skin disorder characterized by keratinocytes hyperproliferation. The IL-23/IL-17 immune pathway has been substantiated in numerous studies to be closely associated with psoriasis progression. Yinxie I Formula is a traditional Chinese medicine made from 9 herbal medicines, which has excellent clinical efficacy in psoriasis. However, to date, the mechanism of action of Yinxie I Formula against psoriasis remains unknown. In this perspective, we discuss the efficacy of Yinxie I Formula in mice with
imiquimod (IMQ) induced psoriasis. Yinxie I Formula significantly reduced the area of skin lesions and the inflammatory response in mice with psoriasis. Furthermore, Yinxie I Formula alleviated the expression levels of inflammation-related genes IL-6, IL-17 A, IL-22, IL-23, TNF-α and IL-23, IL-18, IL-6 and IL-1β-related proteins and alleviated the abnormal surge of dendritic cells, macrophages and T cells in the skin and spleen. Meanwhile we found that Yinxie I Formula reduced the release of NO, TNF-α, IL-1β and IL-23 in lipopolysaccharide-induced mouse macrophage RAW264.7 cell line. The results suggest that the therapeutic mechanism of Yinxie I Formula may also be correlated with the STAT signaling pathway. We further analyzed the active ingredient of Yinxie I Formula, Buddleoside, which may be the main substance that exerts the therapeutic effect. In conclusion, we have investigated that Yinxie I Formula attenuates the IMQ-induced inflammatory response in psoriasis by inhibiting the IL-23/IL-17 axis, which lays the foundation for the antipsoriasis mechanism and provides a theoretical basis for the clinical promotion of Yinxie I Formula.