特应性皮炎样小鼠模型皮肤屏障功能受损的分子机制研究

Study on molecular mechanisms of impaired skin barrier function in an atopic dermatitis-like animal model

目的:建立二硝基氯苯(DNCB)诱导的小鼠AD样模型,观察角质形成细胞的分化和脱落相关基因的表达,探讨皮肤屏障功能受损的分子机制。方法:皮炎组用DNCB两次致敏和两次激发。最后1次致敏后24 h测定各项观察指标。结果:皮炎组小鼠背部经表皮水分丢失量显著高于对照组,角质层含水量显著低于对照组。皮炎组小鼠表皮FLG、IVL、TG-M1荧光强度下降,表皮最外层KLK7荧光强度稍有增强。FLG、IVL、TGM1和KLK7 mRNA的表达出现炎症后修复性改变。结论:DNCB诱导的BALB/c小鼠特应性皮炎样模型存在皮肤屏障功能异常及表皮分化脱落相关基因表达的改变。

Objective： To investigate the molecular mechanisms of impaired skin barrier function in an atopic der- matitis like model of BALB/c mouse induced by 2, 4- dinitrochloro- benzene （DNCB）, through theanalysis of gene expression related to epidermal differentiation and degeneration. Methods： Mice in dermatitis group were sensitized twice and challenged twice with DNCB. Data were obtained 24 hours after the second challenge. Results： Mice in dermatitis group has significandy higher TEWL and lower stratum comeum hydration than control group. The protein expression of FIG, IVL and TGM1 in epidermis was decreased in dermatitis group, and the protein expression of KLK7 in the outermost layer of epidermis was increased in dermatitis group. The mRNA expression of FLG, IVL, TGM1 and KLK7 resembled the changes of repair phase after tissue damage. Conclusion： Skin barrier function of atopic dermatitis like model in BALB/c mouse induced by DNCB was impaired, and there is an alteration of the ex- pression of gene related to epidermal differentiation and degeneration.