背景:特应性皮炎是由遗传易感性引起的常见皮肤病,环境因素,免疫反应,和皮肤屏障功能障碍。山奈酚是一种广泛存在于茶叶中的天然类黄酮,蔬菜,和水果,据报道具有优异的抗炎活性。然而,山奈酚对特应性皮炎的治疗效果尚不清楚。
目的:本研究旨在阐明山奈酚对特应性皮炎皮肤炎症的影响。
方法:使用MC903诱导的特应性皮炎样皮肤炎症小鼠模型检查山奈酚给药对皮肤炎症的抑制作用。对皮肤皮炎和经表皮失水进行定量。进行了组织病理学研究以检查胸腺基质淋巴细胞生成素的表达,角化包膜蛋白,如丝聚蛋白,oricrin,和总蛋白,以及浸润的炎症细胞的数量,包括淋巴细胞,巨噬细胞,和皮炎区的肥大细胞.通过qPCR和使用皮肤组织的流式细胞术分析来研究IL-4和IL-13的表达。通过蛋白质印迹和qPCR研究HO-1的表达。
结果:山奈酚治疗可显著抑制MC903诱导的皮炎,TEWL,TSLP,和HO-1表达,和炎症细胞的浸润。山奈酚治疗可改善聚丝蛋白的表达下降,oricrin,和MC903诱导的皮炎皮肤部位的总蛋白。山奈酚处理的小鼠中IL-4和IL-13的表达部分降低。
结论:山奈酚可能通过抑制2型炎症和抑制TSLP表达和氧化应激改善屏障功能障碍,从而改善MC903诱导的皮炎。山奈酚可能有可能成为特应性皮炎的新疗法。
BACKGROUND: Atopic dermatitis is a common skin disease caused by genetic susceptibility, environmental factors, immune response, and skin barrier dysfunction. Kaempferol is a natural flavonoid widely found in tea, vegetables, and fruits and has been reported to have excellent anti-inflammation activity. However, the therapeutic effect of kaempferol on atopic dermatitis is unclear.
OBJECTIVE: This study aimed to elucidate the effect of kaempferol on skin inflammation in atopic dermatitis.
METHODS: The suppressive effect of kaempferol administration on skin inflammation was examined using
MC903-induced atopic dermatitis-like skin inflammation mouse model. Quantification of skin dermatitis and transepidermal water loss was performed. A histopathological study was performed to examine thymic stromal lymphopoietin expression, cornified envelope proteins such as filaggrin, loricrin, and involucrin, and the numbers of infiltrating inflammatory cells, including lymphocytes, macrophages, and mast cells in the dermatitis area. The expressions of IL-4 and IL-13 were investigated by qPCR and flow cytometry analysis using skin tissues. The expression of HO-1 was investigated by western blot and qPCR.
RESULTS: Kaempferol therapy significantly suppressed
MC903-induced dermatitis, TEWL, TSLP, and HO-1 expression, and infiltration of inflammatory cells. Kaempferol therapy improved the decreased expressions of filaggrin, loricrin, and involucrin in
MC903-induced dermatitis skin site. The expressions of IL-4, and IL-13 were partially decreased in kaempferol-treated mice.
CONCLUSIONS: Kaempferol might improve
MC903-induced dermatitis via suppression of type 2 inflammation and improvement of barrier dysfunction by inhibition of TSLP expression and oxidative stress. Kaempferol might have the potential to be a new treatment for atopic dermatitis.