Takeuchi T, Uitto J, Bernstein E F
Department of Dermatology, Jefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
J Invest Dermatol. 1998 Apr;110(4):343-7. doi: 10.1046/j.1523-1747.1998.00124.x.
Increasing evidence demonstrates that ultraviolet A radiation (UVA) contributes to photoaging, which results in the accumulation of massive amounts of abnormal elastic material in the dermis of photoaged skin. To study UVA-induced photoaging in an in vivo system, we utilized a line of transgenic mice containing the human elastin promoter linked to a chloramphenicol acetyl transferase reporter gene. Our prior work demonstrates promoter activation in response to ultraviolet B radiation (UVB), UVA, and psoralen plus ultraviolet A radiation in the skin of these mice. The addition of psoralen (8-MOP) prior to administration of UVA results in substantial increases in promoter activation, as compared with UVA alone. To demonstrate the utility of these mice as a model of UVA-induced photodamage, we administered four lotions to the skin of our transgenic mice that included: a sunscreen containing octyl methoxycinnamate and benzophenone-3 with a sun protection factor (SPF) of 15, the UVA filter butyl methoxydibenzoylmethane, the SPF 15 sunscreen and the UVA filter together, and the lotion vehicle alone. Following sunscreen administration, mice received a single psoralen plus ultraviolet A radiation treatment. All sunscreens decreased chloramphenicol acetyl transferase activity with the SPF 15 sunscreen, the UVA filter, and the combination SPF 15 sunscreen and UVA filter, resulting in increasing degrees of protection against psoralen plus ultraviolet A radiation. These results demonstrate that this model functions as a rapid and sensitive model of UVA photodamage for the identification and comparison of compounds that protect against UVA-induced photoaging.
越来越多的证据表明，紫外线A辐射（UVA）会导致光老化，这会使光老化皮肤的真皮层中积累大量异常弹性物质。为了在体内系统中研究UVA诱导的光老化，我们使用了一种转基因小鼠品系，该品系含有与氯霉素乙酰转移酶报告基因相连的人弹性蛋白启动子。我们之前的研究表明，在这些小鼠的皮肤中，该启动子会响应紫外线B辐射（UVB）、UVA以及补骨脂素加紫外线A辐射而激活。与单独使用UVA相比，在给予UVA之前添加补骨脂素（8 - MOP）会导致启动子激活显著增加。为了证明这些小鼠作为UVA诱导光损伤模型的实用性，我们给转基因小鼠的皮肤涂抹了四种乳液，分别是：一种含有甲氧基肉桂酸辛酯和二苯甲酮 - 3且防晒系数（SPF）为15的防晒霜、UVA滤光剂丁基甲氧基二苯甲酰甲烷、SPF 15防晒霜和UVA滤光剂的组合，以及单独的乳液载体。涂抹防晒霜后，小鼠接受单次补骨脂素加紫外线A辐射处理。所有防晒霜都降低了氯霉素乙酰转移酶的活性，其中SPF 15防晒霜、UVA滤光剂以及SPF 15防晒霜和UVA滤光剂的组合，对补骨脂素加紫外线A辐射的防护程度依次增加。这些结果表明，该模型可作为一种快速且敏感的UVA光损伤模型，用于鉴定和比较预防UVA诱导光老化的化合物。
