CAJ | 학술논문

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.
목적 탐토부서지산유고외용대병장수손적피부염증반응적작용.방법 웅성SKH-1무모소서8지,재매지소서배부표기6개1 cm×2 cm적실험구,분위6조:분별위공백대조조、병장파배조、병장파배+부서지산조、병장파배+기질조、병장완정+부서지산조、병장완정+기질조.채용효대시탈법거제각질층표피지질,건립급성병장공능손상적동물모형.국부외용부서지산유고혹기질,12 h후대수시부위진행균락채집감정,병취피부표본채용실시형광정량PCR검측피부중수양분화인자88(MyD88)화백세포개소(IL)-1α、IL-6이급표피항균태S100a8화S100a9적표체.결과 병장파배조MyD88 mRNA표체(8.3±3.0)위공백대조조(0.8±0.4)적8배,기IL-1α、IL-6급S100a8화S100a9 mRNA표체균고우공백대조조.병장파배+부서지산조여병장파배조비교,IL-1α mRNA수평현저하강(2.8±0.3비20.1±10.0,F=47.11,P＜ 0.01),IL-6수평현저하조(1.6±2.3비9.4±4.0,F=16.18,P＜ 0.01),S100a8 mRNA수평현저하강(1.5±1.4비5.0±1.6,F=59.71,P＜ 0.05),S100a9 mRNA역현저하강(1.2±0.7비3.4±1.6,F=21.94,P＜ 0.05).결론 부서지산유고외용대우병장손상후적염증반응유명현적억제작용,가능위기치료염증성피부병적작용궤제지일.
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,barrierunimpaired 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.