環境中過敏原、輻射、物理或化學性刺激，都可能引發過敏性接觸皮膚炎(Allergic contact dermatitis)，接觸性過敏原基本上是小分子可溶性半抗原誘發，之前研究報告指出在動物施予oxazolone可誘導皮膚發炎，病灶釋放出與臨床患者身上所測得的相似的發炎因子，本研究挑選oxazolone作為誘導劑建構過敏性接觸皮膚炎的實驗動物模型。中醫臨床用藥荊芥(Schizonepeta tenuifolia)，在中國常被用於感冒、發燒、麻疹等治療，荊芥的乙醇提取物，具備鎮痛和顯著的抗發炎作用。
本研究以5%的oxazolone塗抹ICR小鼠的背部皮膚誘發過敏反應，5天後再施以1%的oxazolone作為發炎刺激，小鼠產生皮膚紅、腫、脫皮等過敏性接觸皮膚炎的症狀，塗抹荊芥乙醇水提取液後顯著改善老鼠皮膚發炎的作用。進一步利用HaCaT細胞探討oxazolone誘導的損傷及發炎機制，細胞實驗結果顯示胞內ROS升高，過多ROS導致IκB磷酸化降解現象，釋放NF-κB，活化NF-κB轉位入細胞核，轉錄調控TNF-α、IL-8等發炎因子表現。本研究並證實荊芥的乙醇水提取物可以調降oxazolone誘發的ROS濃度、抑制IκB磷酸化並減弱角質細胞中NF-κB的表達，減緩HaCaT cells的氧化損傷，荊芥亦調降TNF-α、IL-8細胞激素的表達。
Contact dermatitis is a frequent inflammatory skin disease induced by skin exposure to low molecular weight chemicals. Previous studies have reported that administered the oxazolone hapten can induce skin inflammation in animals. Nevertheless, oxazolone-challenged skin lesions in mouse induced structural, immunologic and biochemical similarities with human dermatitis. In the present study, we examined the inhibitive effect of Schizonepeta tenuifolia on oxazolone-induced dermatitis-like skin lesions in hairless mice. Schizonepeta tenuifolia is of the Labiatae family of plants commonly used in China for the treatment of colds, fever and measles.
In this study, oxazolone challenged hairless mice were used to evaluate if Schizonepeta can alleviate dermatitis as determined by clinical signs, histology, cytokine (IL-8 and TNF-α). The administration of Schizonepeta significantly improved skin symptoms both at the scaling and erosion/excoriation/hemorrhage. H&E staining of dorsal skin showed that Schizonepeta inhibited the infiltration of CD3 and CD45 positive inflammatory cells. Oxazolone-induced production of ROS and mitoROS were decreased upon the Schizonepeta treatment. The extract of Schizonepeta suppressed the generation of TNF-α and IL-8 as well as attenuated the activation of NF-κB in in HaCaT cells. Our data suggested that Schizonepetae may protect skin cells against oxazolone-induced inflammation and dermatitis by modulating ROS concentration and p-Iκb/NF-κB signal transduction pathways.
