Archive > Volume 17 Issue 2 > 2025,17(2):368-379. DOI:https://doi.org/10.1016/j.chmed.2024.01.003 Prev Next

蛇床子素通过抑制IL-31改善DNCB诱导的小鼠特应性皮炎慢性瘙痒

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Osthole ameliorates chronic pruritus in 2,4-dichloronitrobenzeneinduced atopic dermatitis by inhibiting IL-31 production

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    摘要:
    目的：特应性皮炎（atopic dermatitis，AD）是一种以炎症、湿疹样病变和瘙痒为典型症状的慢性皮肤病。传统中药蛇床子的关键成分蛇床子素能够缓解瘙痒和抑制炎症，但蛇床子素作用于AD的具体机制尚不明确。 方法：本研究探讨了蛇床素在2,4-二硝基氯苯（2,4-dichloronitrobenzen，DNCB）构建的AD小鼠模型及肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）和干扰素-γ（interferon-γ，IFN-γ）诱导的HaCaT炎症细胞模型中的抗炎作用。并评估了蛇床子素抑制AD小鼠模型瘙痒行为的作用。采用了苏木精-伊红（hematoxylin and eosin，HE）染色、酶联免疫吸附测定（enzyme-linked immunosorbent assay，ELISA）、蛋白质免疫印迹（western blot，WB）、定量实时PCR（quantitative real-time PCR，qRT-PCR）和免疫荧光染色等实验方法。 结果：蛇床子素通过缓解皮肤损伤、降低皮损评分、减少抓挠次数和降低表皮厚度改善了小鼠的AD样症状。此外，蛇床子素还降低了皮肤组织和HaCaT细胞中白细胞介素（interleukin，IL）-31及IL-31受体A（IL-31 receptor A，IL-31 RA）的水平，抑制了p65和IκBα蛋白的磷酸化水平。并且，在HaCaT细胞中，蛇床子素上调了过氧化物酶体增殖激活受体（peroxisome proliferator-activated receptor，PPAR）α和PPARγ的蛋白表达水平。 结论：结果表明，蛇床素通过激活PPARα、PPARγ，抑制NF-κB信号通路的激活以及IL-31和IL-31 RA的表达，有效抑制了AD慢性瘙痒。

    Abstract:
    Objective: This study aims to elucidate the therapeutic potential of osthole for the treatment of atopic dermatitis (AD), focusing on its ability to alleviate chronic pruritus (CP) and the underlying molecular mechanisms. Methods: In this study, we investigated the anti-inflammatory effects of osthole in both a 2,4- dichloronitrobenzene (DNCB)-induced AD mouse model and tumor necrosis factor-a (TNF-a) and interferon-c (IFN-c) stimulated human immortalized epidermal (HaCaT) cells. The anti-itch effect of osthole was specifically assessed in the AD mouse model. Using methods such as hematoxylin and eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), western blot (WB), quantitative real-time PCR (qRT-PCR), and immunofluorescence staining. Results: Osthole improved skin damage and clinical dermatitis scores, reduced scratching bouts, and decreased epidermal thickness AD-like mice. It also reduced the levels of interleukin (IL)-31 and IL-31 receptor A (IL-31 RA) in both skin tissues and HaCaT cells. Furthermore, Osthole suppressed the protein expression levels of phosphor-p65 (p-p65) and phosphor-inhibitor of nuclear factor kappa-Ba (p-IjBa). Meanwhile, it increased the protein expression levels of peroxisome proliferator-activated receptor a (PPARa) and PPARc in HaCaT cells. Conclusion: These findings indicated that osthole effectively inhibited CP in AD by activating PPARa, PPARc, repressing the NF-jB signaling pathway, as well as the expression of IL-31 and IL-31 RA.

    关键词:
    特应性皮炎;慢性瘙痒;蛇床子;白介素-31;NF-κB;蛇床子素;过氧化物酶体增殖物激活受体

    Keywords:


    Project Supported:
    This work was supported by the Natural Science Foundation of China (NSFC) to Guanyi Wu (No. 82060768); the Natural Science Foundation of Guangxi Zhuang Autonomous Region (No. 2020GXNSFAA297244); Innovation Project of Guangxi Graduate Education (No. YCSW2023392); an Open Project of the Guangxi University of Chinese Medicine Top Disciplines Construction Project (No. 2018XK022); an Open Project of the Guangxi Key Laboratory of Zhuang and Yao Ethnic Medicine (No. GXZYKF2020-07); Guipai Traditional Chinese Medicine Top-Notch Talent Funding Project from Guangxi University of Chinese Medicine (No. 2022C001); the Second and Third Batch of the ‘‘Qihuang Project” High-Level Talent Team Cultivation Project of Guangxi University of Traditional Chinese Medicine (No. 2021001 and No. 202402).

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