目的：构建光敏剂结合 UVA 诱导的小鼠皮肤光老化模型。方法： ICR 小鼠分为3组：模型组外用1％甲氧沙林溶液(8-M。P)后进行 UVA 照射、单纯 UVA 照射组和空白对照组。照射后观察皮肤外观表现、病理学变化和超微结构特点,确定各组诱导皮肤光老化进程的累积照射剂量和时间。结果：单纯 UVA 照射组在第45天,UVA 剂量约720 J/ cm2时,肉眼观察皮肤外观、组织病理方面和超微结构都呈现比较典型的光老化表现；模型组(8-M。P / UVA)小鼠在第3天,UVA 累积剂量约47 J/cm2时,透射电镜下可见角质形成细胞和基底层黑素细胞的显著凋亡(核固缩)；第5天,UVA 累积剂量约78 J/ cm2时,病理示：真皮层部分弹性纤维变性；随着照射剂量的增加,第6天 UVA 累积剂量达95 J/ cm2时,出现典型的光老化表现,透射电镜下可清晰观察到弹性纤维和胶原蛋白束的病理改变。结论：8-M。P / UVA 可以快速诱导小鼠皮肤光老化模型的建立。%Objective: To construct a mice photoaging model induced by photosensitizer combined with ul-traviolet A (UVA). Methods: The ICR mice were divided into three groups: In group one the mice were trea-ted with topical 1% methoxypsoralen (8-MOP) solution plus repeated UVA exposure, (8-MOP / UVA); In group two, only repeated UVA irradiation was used and group three was blank control group. After irradiation, by observing the clinical, pathological and ultrastructural features in different stage, photoaging process were correlated with cumulative radiation dose and time. Results: In group two when the UVA dose was about 720 J/ cm2 at the day 45, the clinical manifestations, pathology and ultrastructure showed typical manifestation of photoaging. In group one (8-MOP / UVA group) at the time of the day 3, with UVA dose about 47 J/ cm2 , al-though no clinical changes were found, mild broken and twisted elastic fibers at the superficial dermis and also numerous apoptotic keratinocytes and melanocytes were seen under both light microscope and transmission e-lectron microscope (TEM). Clinical changes occurred at day 5 with accumulated UVA dose about 78 J/ cm2 , presented with dull skin, fine lines, mottled pigmentation, accompanied by obvious degeneration of elastic fi-bers in the dermis. On day 6 with UVA dose about 95 J/ cm2 ,typical clinical feature of photoaging with coarse transverse wrinkles, and pathologically large proportion of elastic fibers degenerated were presented, especially under TEM. Conclusion: An animal model for photoaging can be quickly induced by 8-MOP / UVA.
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