低温治疗通过p38 MAPK信号通路抑制UVB诱导的小鼠皮肤炎症

Cold therapy prevents UVB-induced inflammation through p38 MAPK signaling pathways in mouse skin

目的探讨局部低温治疗对中波紫外线辐射(UVB)诱导的皮肤炎症的作用机制。方法角质形成细胞体外培养后接受如下3种处理:仅低温治疗、仅UVB照射、UVB照射后低温治疗,检测低温治疗对UVB照射后角质形成细胞的作用。将野生型雌性C57BL/6小鼠分为3组:低温治疗组、UVB组、UVB+低温治疗组。通过数字测微计测量、组织病理学、免疫组织化学、免疫荧光、定量RT-PCR和Western blot检测低温治疗对UVB诱导炎症的影响。结果低温治疗可显著减少UVB诱导的巨噬细胞和T细胞浸润(P<0.05),并显著抑制UVB诱导的p38磷酸化(P<0.05),减少相关的炎症反应,包括减轻耳肿胀反应、表皮增生(P<0.05)和皮肤炎症(P<0.05),减少小鼠模型中相关细胞因子表达和细胞凋亡(P<0.05)。结论低温治疗是治疗UVB诱导的皮肤炎症的一种有效的方法。

This study was designed to explore the effects of local cold therapy on ultraviolet radiation B(UVB)-induced skin inflammation.Cultured keratinocytes were subjected respectively to cold therapy,UVB irradiation and UVB irradiation+cold therapy,to detect the effects of cold therapy on keratinocytes after UVB irradiation.Wildtype female C57BL/6 mice were divided into cold therapy group,UVB group and UVB+cold therapy group to detect the effects of cold therapy on UVB-induced inflammation by means of digital micrometer measurement,histopathology,immunohistochemistry,immunofluorescence,quantitative RT-PCR,and Western blotting.Data showed that cold therapy could significantly reduce UVB-induced macrophages and T cells infiltration,significantly inhibit UVB-induced phosphorylation of p38,reduce related inflammatory responses,including the alleviation of ear-swelling response,epidermal hyperplasia and cutaneous inflammation,and reduce relative cytokine expression and cell apoptosis in mice model.Collectively,cold therapy could be an effective modality treatment for UVB-induced skin inflammation.