Starcher B, Conrad M
Department of Biochemistry, University of Texas Health Center at Tyler 75710, USA.
Ciba Found Symp. 1995;192:338-46; discussion 346-7.
Hairless (SKH-1) mice were mated with beige (C57BL/bb) mice to produce a hairless mouse deficient in neutrophil elastase (hhbb). These mice were exposed to 0.09 J UVB radiation for 5 months to see if neutrophil elastase was an important factor in the development of solar elastosis. Analysis of peritoneal neutrophils confirmed that the hhbb mouse was deficient in elastase, retaining only 10% of the activity of the normal littermates (hhHb). Skin myeloperoxidase activity was equally elevated in all the mice receiving UVB indicating a similar influx of inflammatory cells. The absolute breaking strength of the skin in both the hhBb and hhbb mice was not altered by UVB treatment over the 5 month exposure period. Elastin quantitated biochemically as desmosine, or visualized histologically, was increased following UVB exposure in the normal mice. In the elastase-deficient mice, however, the elastin fibres appeared to be unaffected by exposure to UVB radiation at this level. The results suggest that neutrophil elastase is an important mediator in the development of solar elastosis resulting from continued exposure to UVB.
无毛（SKH - 1）小鼠与米色（C57BL/bb）小鼠交配，以产生缺乏中性粒细胞弹性蛋白酶的无毛小鼠（hhbb）。将这些小鼠暴露于0.09焦耳的紫外线B辐射下5个月，以观察中性粒细胞弹性蛋白酶是否是日光性弹力组织变性发展中的一个重要因素。对腹腔中性粒细胞的分析证实，hhbb小鼠缺乏弹性蛋白酶，其活性仅为正常同窝小鼠（hhHb）的10%。所有接受紫外线B照射的小鼠皮肤髓过氧化物酶活性均同样升高，表明炎症细胞的流入相似。在5个月的暴露期内，紫外线B处理并未改变hhBb和hhbb小鼠皮肤的绝对断裂强度。通过生化方法定量为锁链素的弹性蛋白，或通过组织学观察，在正常小鼠接受紫外线B照射后增加。然而，在弹性蛋白酶缺陷小鼠中，这个水平的紫外线B辐射似乎并未影响弹性纤维。结果表明，中性粒细胞弹性蛋白酶是持续暴露于紫外线B导致日光性弹力组织变性发展中的一个重要介质。
