中华皮肤科杂志 ›› 2014, Vol. 47 ›› Issue (12): 864-867.

• 论著 • 上一篇    下一篇

夫西地酸乳膏对小鼠急性皮肤屏障损伤引起炎症反应的抑制作用

仲少敏1,郭建美2,陶荣2,孙楠1,吴艳1   

  1. 1. 北京大学第一医院皮肤科
    2. 北京大学第一医院
  • 收稿日期:2014-03-09 修回日期:2014-08-13 出版日期:2014-12-15 发布日期:2019-06-14
  • 通讯作者: 吴艳 E-mail:3437477565@qq.com

Inhibitory effect of fusidic acid cream on inflammatory reaction caused by acute skin barrier damage in mice

  • Received:2014-03-09 Revised:2014-08-13 Online:2014-12-15 Published:2019-06-14
  • Contact: 艳 吴 E-mail:3437477565@qq.com

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摘要： 目的 探讨夫西地酸乳膏外用对屏障受损的皮肤炎症反应的作用。 方法 雄性SKH-1无毛小鼠8只，在每只小鼠背部标记6个1 cm × 2 cm的实验区，分为6组：分别为空白对照组、屏障破坏组、屏障破坏 + 夫西地酸组、屏障破坏 + 基质组、屏障完整 + 夫西地酸组、屏障完整 + 基质组。采用胶带撕脱法去除角质层表皮脂质，建立急性屏障功能损伤的动物模型。局部外用夫西地酸乳膏或基质，12 h后对受试部位进行菌落采集鉴定，并取皮肤标本采用实时荧光定量PCR检测皮肤中髓样分化因子88（MyD88）和白细胞介素（IL）-1α、IL-6以及表皮抗菌肽S100a8和S100a9的表达。 结果 屏障破坏组MyD88 mRNA表达（8.3 ± 3.0）为空白对照组（0.8 ± 0.4）的8倍，其IL-1α、IL-6及S100a8和S100a9 mRNA表达均高于空白对照组。屏障破坏 + 夫西地酸组与屏障破坏组比较，IL-1α mRNA水平显著下降（2.8 ± 0.3比20.1 ± 10.0，F = 47.11，P < 0.01），IL-6水平显著下调（1.6 ± 2.3比9.4 ± 4.0，F = 16.18，P < 0.01），S100a8 mRNA水平显著下降（1.5 ± 1.4比5.0 ± 1.6，F = 59.71，P < 0.05），S100a9 mRNA亦显著下降（1.2 ± 0.7比3.4 ± 1.6，F = 21.94，P < 0.05）。 结论 夫西地酸乳膏外用对于屏障损伤后的炎症反应有明显的抑制作用，可能为其治疗炎症性皮肤病的作用机制之一。

关键词: 梭链孢酸, 皮肤屏障, 髓样分化因子88, 白细胞介素类

Abstract: Zhong Shaomin, Guo Jianmei, Tao Rong, Sun Nan, Wu Yan. Department of Dermatology, Peking University First Hospital, Beijing 100034, China Corresponding author: Wu Yan, Email: adelewu@medmail.com.cn 【Abstract】 Objective To investigate the effect of fusidic acid cream on inflammatory reaction caused by skin barrier damage. Methods Eight male SKH-1 hairless mice were included in this study. The back of each of these mice were equally divided into six regions measuring 1 cm × 2 cm in size, which were then assigned into six groups: blank control group remaining untreated, barrier-impaired group, barrier-impaired and fusidic acid-treated group, barrier-impaired and vehicle-treated group, barrier-unimpaired and fusidic acid-treated group, barrier-unimpaired and vehicle-treated group. Stratum corneum was removed by adhesive tape stripping to establish an animal model of acute skin barrier damage in the corresponding skin regions of these mice, and fusidic acid cream or vehicle was topically applied to the corresponding regions once. Twelve hours later, skin surface swab samples were collected from the back of these mice followed by bacterial culture and colony counting. Mice were then sacrificed, and skin tissue specimens were resected from these mice, and subjected to real-time fluorescence-based quantitative PCR for the measurement of the mRNA expressions of myeloid differentiation factor 88 （MyD88）, interleukin-1α （IL-1α）, IL-6, epidermal antibacterial peptides S100a8 and S100a9. Statistical analysis was carried out by repeated-measures analysis of variance （ANOVA） and least significant difference （LSD） test. Results The mRNA expressions of MyD88, IL-1α, IL-6, S100a8 and S100a9 were all significantly higher in the barrier-impaired group than in the blank control group （all P < 0.05）. Specifically, the mRNA expression level of MyD88 in the barrier-impaired group was 8 times that in the blank control group （8.3 ± 3.0 vs. 0.8 ± 0.4）. Compared with the barrier-impaired group, the barrier-impaired and fusidic acid-treated group showed a significant decrease in the mRNA expressions of IL-1α （2.8 ± 0.3 vs. 20.1 ± 10.0, F = 47.11, P < 0.01）, IL-6 （1.6 ± 2.3 vs. 9.4 ± 4.0, F = 16.18, P < 0.01）, S100a8 （1.5 ± 1.4 vs. 5.0 ± 1.6, F = 59.71, P < 0.05） and S100a9 （1.2 ± 0.7 vs. 3.4 ± 1.6, F = 21.94, P < 0.05）. Conlusions Fusidic acid cream could attenuate the inflammatory reaction caused by acute skin barrier damage, which might partly explain its action mechanism in the treatment of inflammatory skin diseases.

Key words: Fusidic acid, Skin barrier, Myeloid differentiation factor 88, Interleukins