中性粒细胞弹性蛋白酶在太阳弹性症中的作用。

B. Starcher, M. Conrad
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引用次数: 35

摘要

无毛(SKH-1)小鼠与米色(C57BL/bb)小鼠交配,产生中性粒细胞弹性酶(hhbb)缺乏的无毛小鼠。这些小鼠暴露在0.09 juvb辐射下5个月,以观察中性粒细胞弹性蛋白酶是否是太阳弹性病发生的重要因素。腹膜中性粒细胞分析证实hhbb小鼠缺乏弹性蛋白酶,仅保留正常窝鼠10%的活性(hhHb)。在所有接受UVB的小鼠中,皮肤髓过氧化物酶活性都同样升高,表明炎症细胞的流入相似。在5个月的暴露期内,hhBb和hhBb小鼠皮肤的绝对断裂强度没有被UVB处理改变。在正常小鼠中波紫外线照射后,弹性蛋白被生化定量为桥糖素,或在组织学上可见。然而,在弹性蛋白缺乏的小鼠中,弹性蛋白纤维似乎不受暴露在这个水平的UVB辐射的影响。结果表明,中性粒细胞弹性蛋白酶在持续暴露于UVB引起的太阳弹性症的发展中起着重要的中介作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A role for neutrophil elastase in solar elastosis.
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.
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