摘要
目的 探讨抗光敏合剂对皮肤光损伤的作用机制.方法 以300 mJ/cm2UVB辐射BALB/c小鼠建立急性光损伤的模型,在预防性应用中药抗光敏合剂后,与正常小鼠、预防性应用生理氯化钠溶液及羟氯喹小鼠,进行平行对照研究.结果 与正常小鼠比较,急性光损伤小鼠Fas和Caspase-3表达明显升高,细胞凋亡指数上升(P值均<0.01).与生理氯化钠溶液相比,中药抗光敏合剂可以抑制紫外线照射诱导的角质形成细胞Caspase-3活性升高,同时下调Fas表达,并抑制角质形成细胞凋亡(P值<0.01或0.05).结论 抗光敏合剂可缓解紫外线引起的表皮角质形成细胞炎性损害和细胞凋亡状态,其保护作用机制与调节细胞凋亡的Caspase-3通路相关.
Objective To investigate the action mechanism of an anti-photosensitivity mixture on skin photodamage. Methods Twenty-eight BLAB/c mice were divided into 4 groups, i.e., normal control group,treatment group, negative and positive control groups; the last three groups were irradiated with a single dose of UVB at 300 mJ/cm2 after 7-day pretreatment with sodium chloride physiological solution, anti-photosensitivity mixture, and hydroxychloroquine, respectively. Twenty-four hours after the irradiation, mice were killed and skin tissue samples were obtained at the irradiated sites. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) and immunohistochemical staining were carried out to detect cell apoptosis,Fas and Caspase-3 protein expressions respectively. Results An increase was observed in the expression level of Fas and Caspase-3 and in the apoptotic index in keratinocytes from UV-irradiated mice compared with unirradiated control mice (all P < 0.01 ). In comparison with sodium chloride physiological solution, the antiphotosensitivity mixture suppressed the UV irradiation-induced increase in the expression intensity of Fas and Caspase-3 and apoptotic index in keratinocytes (P < 0.05 or 0.01 ). Conclusions The anti-photosensitivity mixture could alleviate UV-induced inflammatory damage to and apoptosis in epidermal keratinocytes, likely by regulating cell apoptosis and Caspase-3 pathway.
出处
《中华皮肤科杂志》
CAS
CSCD
北大核心
2011年第2期138-140,共3页
Chinese Journal of Dermatology
基金
北京市教育委员会科技计划课题(KM200910025026)
北京市优秀人才资助项目(2009D003007000001)