CAJ | 학술논문

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.
목적 탐토항광민합제대피부광손상적작용궤제.방법 이300 mJ/cm2UVB복사BALB/c소서건립급성광손상적모형,재예방성응용중약항광민합제후,여정상소서、예방성응용생리록화납용액급간록규소서,진행평행대조연구.결과 여정상소서비교,급성광손상소서Fas화Caspase-3표체명현승고,세포조망지수상승(P치균＜0.01).여생리록화납용액상비,중약항광민합제가이억제자외선조사유도적각질형성세포Caspase-3활성승고,동시하조Fas표체,병억제각질형성세포조망(P치＜0.01혹0.05).결론 항광민합제가완해자외선인기적표피각질형성세포염성손해화세포조망상태,기보호작용궤제여조절세포조망적Caspase-3통로상관.
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.