皮肤光老化动物模型的建立

目的:应用中波紫外线(UVB 290-320nm)照射无毛鼠,观察UVB对无毛鼠皮肤纹理、表皮、及真皮基质的影响,建立皮肤光老化动物模型,为临床防治皮肤光老化打下基础。方法:应用皮肤图像分析系统、皮肤组织学及特殊染色方法,对接受中波紫外线照射20周的无毛鼠进行皮肤纹理、表皮、真皮、基底膜、粘多糖、胶原纤维、弹性纤维进行对比观察。结果:无毛鼠经UVB照射20周、总计量5.9J/cm2,皮肤出现粗糙,皮纹加深、加宽。皮肤增厚,表皮增生、伴有角化过度及角化不全。真皮水肿,纤维母细胞增生,弥漫性单核细胞、肥大细胞、嗜中性白细胞侵润。基底膜不规则增厚。胶原含量减少,染色变浅,胶原纤维明显变性,均质化,形成片、块状,变性的胶原纤维延伸至真皮深层。弹性纤维增多变粗,部分增生的弹性纤维聚集、断裂、缠结。结论:中波紫外线引起的皮肤损害是一个慢性炎症过程。真皮及真皮基质的改变是紫外线引起皮肤光老化的病理基础。中波紫外线照射后的无毛鼠的皮肤所发生的变化与临床皮肤光老化疾病一致,因此该模型是较为理想的研究皮肤光老化的动物模型。

The Construction of Photoaged Skin Animal Model

Objective: To treat and prevent photoaging in humans, hairless mice were exposed to ultraviolet B(UVB290-320nm) to study skin changes in stigmata, epidermis, dermis, dermal structural elements, these changes are similar to humans induced by chronic ultraviolet. Methods: Twenty hairless mice were exposed in ultraviolet B (UVB) for 20 weeks, total dose 5.9J/cm2. After irradiation, the dorsal skin of animals were analysed by computer imaging analysis system, histological and specific strains. Result: Hairless skin in ultraviolet irradiated, the stigmata are coarse, deepening wrinkles, the epidermis became hyperplastic and skin thickened. Dermal-epidermal basement membrane was thick and un-regular. PAS positive substances were increased. Fibroblasts were increased. Mononuclear cells infiltrated into the dermis. The content of collagen was decreased. Elastic fibers were thickened, proliferated and coalesced into extensive denaturalization. Conclusion: Chronic exposure of hairless mice to ultraviolet B is associated with inflammation. The changes of dermis and dermal structural elements are pathologic bases of photoaged skin. So this model is a perfect photoaged animal model.