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银屑 I 方通过 IL-23/IL-17 轴减轻咪喹莫特诱导的银屑病样皮肤炎症。

Yinxie I Formula attenuates imiquimod-induced psoriasis-like skin inflammation via IL-23/IL-17 axis.

机构信息

Department of Dermatology, General Hospital of Ningxia Medical University, No. 804 Shengli Street, Yinchuan, 750004, Ningxia Hui Autonomous Region, PR China.

Ningxia Medical University, Yinchuan, 750004, Ningxia Hui Autonomous Region, PR China.

出版信息

Arch Dermatol Res. 2024 Aug 19;316(8):540. doi: 10.1007/s00403-024-03288-3.

Abstract

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.

摘要

银屑病被认为是一种慢性炎症性皮肤病,其特征是角质形成细胞过度增殖。大量研究证实,IL-23/IL-17 免疫途径与银屑病的进展密切相关。银屑 I 号方是一种由 9 种草药组成的中药,对银屑病具有良好的临床疗效。然而,迄今为止,银屑 I 号方治疗银屑病的确切作用机制尚不清楚。在本研究中,我们探讨了银屑 I 号方对咪喹莫特(IMQ)诱导的银屑病小鼠的疗效。银屑 I 号方显著减轻了银屑病小鼠的皮肤损伤面积和炎症反应。此外,银屑 I 号方减轻了炎症相关基因 IL-6、IL-17A、IL-22、IL-23、TNF-α 和 IL-23、IL-18、IL-6 和 IL-1β相关蛋白的表达水平,并减轻了皮肤和脾脏中树突状细胞、巨噬细胞和 T 细胞的异常激增。同时我们发现,银屑 I 号方可降低脂多糖诱导的小鼠巨噬细胞 RAW264.7 细胞系中 NO、TNF-α、IL-1β和 IL-23 的释放。结果表明,银屑 I 号方的治疗机制可能也与 STAT 信号通路有关。我们进一步分析了银屑 I 号方的活性成分,梓醇,它可能是发挥治疗作用的主要物质。综上所述,我们研究发现银屑 I 号方可通过抑制 IL-23/IL-17 轴减轻 IMQ 诱导的银屑病炎症反应,为银屑病的治疗机制奠定了基础,并为银屑 I 号方的临床推广提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ba/11333517/a282ff352524/403_2024_3288_Fig1_HTML.jpg

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