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首页> 外文期刊>Journal of dermatological science >Effect of dehydroepiandrosterone on atopic dermatitis-like skin lesions induced by 1-chloro-2,4-dinitrobenzene in mouse
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Effect of dehydroepiandrosterone on atopic dermatitis-like skin lesions induced by 1-chloro-2,4-dinitrobenzene in mouse

机译：脱氢表雄酮对1-氯-2,4-二硝基苯致小鼠特应性皮炎样皮肤损伤的影响

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Background: Th2 cells are overexpressed in the skin and serum of atopic dermatitis (AD) patients. Previously, we found that dehydroepiandrosterone (DHEA) decreased eosinophil infiltration in asthmatic mice through the suppression of Th2-associated cytokines. Therefore, we hypothesized that DHEA might improve the symptoms of AD syndrome. Objective: In this study, we evaluated the symptom improvement and anti-inflammatory response that result from the modulation of immunity by DHEA modulated in AD-like mice. Methods: Female BALB/c mice were sensitized and challenged with 1-chloro-2,4-dinitrobenzene. On days 14-29 after sensitization, mice were treated with cutaneous (skin smear) or oral administration of DHEA. In addition, human keratinocyte (HaCat) cells were used to evaluate the effect of DHEA on the in vitro production of proinflammatory cytokines and chemokines. Results: Both cutaneous and oral DHEA were able to decrease ear swelling and skin inflammation in AD-like mice. DHEA also attenuated eosinophil and mast cell infiltration into ear and skin tissue. Additionally, Th2-associated cytokines were inhibited in splenocyte culture, and suppressed the levels of IgE and interleukin 4 in serum. Oral and cutaneous administration of DHEA reduced the inflammatory response, as evidenced by AD-like skin lesions, in a similar manner. DHEA significantly reduced inflammatory cytokines and chemokines through the nuclear factor-κB and mitogen-activated protein kinases pathways in tumor necrosis factor-α activated HaCat cells. Conclusion: DHEA ameliorates AD-like mouse skin inflammation and reduces eosinophil and mast cell infiltration by reducing the production of Th2-associated cytokines and chemokines.
机译：背景：Th2细胞在特应性皮炎（AD）患者的皮肤和血清中过表达。以前，我们发现脱氢表雄酮（DHEA）通过抑制Th2相关细胞因子来减少哮喘小鼠的嗜酸性粒细胞浸润。因此，我们假设DHEA可能会改善AD综合征的症状。目的：在这项研究中，我们评估了由ADEA小鼠中DHEA调节免疫力引起的症状改善和抗炎反应。方法：用1-氯-2,4-二硝基苯敏化并攻击雌性BALB / c小鼠。在致敏后的第14-29天，用皮肤（皮肤涂片）或口服DHEA治疗小鼠。此外，人类角质形成细胞（HaCat）被用于评估DHEA对促炎细胞因子和趋化因子的体外产生的影响。结果：皮肤和口服脱氢表雄酮均能够减轻AD样小鼠的耳肿胀和皮肤炎症。 DHEA还减弱了嗜酸性粒细胞和肥大细胞向耳和皮肤组织的浸润。此外，Th2相关的细胞因子在脾细胞培养中被抑制，并抑制血清中IgE和白介素4的水平。 DHEA的口服和皮肤给药以类似的方式降低了炎症反应，如AD样皮肤病变所证明的。 DHEA通过肿瘤坏死因子-α激活的HaCat细胞中的核因子-κB和丝裂原激活的蛋白激酶途径显着减少了炎症细胞因子和趋化因子。结论：DHEA通过减少Th2相关细胞因子和趋化因子的产生，改善了AD样小鼠的皮肤炎症，并减少了嗜酸性粒细胞和肥大细胞的浸润。

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