中华皮肤科杂志 ›› 2011, Vol. 44 ›› Issue (3): 178-181.

• 论著 • 上一篇    下一篇

不同剂量UVA1辐射对硬皮病鼠模型皮肤匀浆CD34和M30的影响

鞠梅1,陈崑1,常宝珠1,顾恒2   

  1. 1. 南京 中国医学科学院北京协和医学院皮肤病研究所
    2. 中国医学科学院皮肤病医院（研究所）理疗科
  • 收稿日期:2010-06-24 修回日期:2010-11-15 出版日期:2011-03-15 发布日期:2011-03-10
  • 通讯作者: 顾恒 E-mail:guhengy@yahoo.com.cn

Effects of different doses of UVA1 irradiation on the expressions of CD34 and M30 in skin homogenate from a mouse model of scleroderma

2, 2,   

  • Received:2010-06-24 Revised:2010-11-15 Online:2011-03-15 Published:2011-03-10

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摘要：

目的 比较硬皮病鼠模型经不同剂量UVA1辐射后皮肤匀浆中CD34和M30的变化，初步探讨UVA1光疗法对硬皮病血管内皮细胞功能的影响。方法 建立硬皮病鼠模型，并随机分为模型对照组、UVA1照射组（按剂量又分为100 J/cm2、60 J/cm2、20 J/cm2组，每周照射3次，共10周）及未照射组，每组10只，共50只。治疗结束后处死小鼠，取背部造模处皮肤一份行组织病理检查，另一份制成5%匀浆，ELISA法检测各组小鼠皮肤匀浆中CD34和M30含量。结果 UVA1照射组小鼠治疗30次后，肉眼观察皮肤变软、变薄，以100 J/cm2组改变最为明显；组织病理见小鼠真皮厚度变薄，胶原无明显增生，皮下脂肪层内见毛囊结构。未照射组皮肤匀浆中CD34、M30含量分别为（22.25 ± 8.91） μg/L和（162.41 ± 58.00） U/L，模型组分别为（31.97 ± 17.97） μg/L和（195.71 ± 71.09） U/L。UVA1组皮肤匀浆中CD34含量增加，M30含量降低，以100 J/cm2 UVA1组的改变最为明显，分别为（72.39 ± 13.04） μg/L和（38.06 ± 19.89） U/L，与模型组及未照射组比较，差异均有统计学意义（P < 0.01）。不同剂量UVA1照射组间经单因素方差分析，FCD34 = 21.23，P < 0.01，FM30 = 15.32，P < 0.01，三组间差异均有统计学意义。结论 UVA1光疗法可上调硬皮病小鼠皮肤CD34，降低M30含量，且其作用与照射强度、累积剂量有关。

关键词: 血管内皮细胞

Abstract:

Objective To observe the expression changes of CD34 and M30 in skin homogenate from a mouse model of scleroderma after irradiation with different doses of UVA1, and to investigate the effect of UVA1 phototherapy on vascular endothelial cell function in scleroderma. Methods The experimental mouse models of scleroderma were established by the injection with bleomycin and randomly divided into model control group （n = 10）, UVA1 irradiation group （n = 30） and unirradiated group （n = 10）. The UVA1 irradiation group was further equally divided into 3 groups, HD-UVA1 group irradiated with UVA1 at 100 J/cm2, MD-UVA1 group with UVA1 at 60 J/cm2, and LD-UVA1 group with UVA1 at 20 J/cm2; phototherapy was performed thrice weekly for 10 weeks followed by the sacrifice of mice. The mice in model control group were killed immediately after the establishment of models, and the mice in unirradiated group received no irradiation after the establishment of models and were maintained till the killing of mice in UVA1 irradiation groups. Skin specimens were obtained from the bleomycin-induced scleroderma lesions of mice and separated into two parts, one was subjected to histopathological examination, and the other one was used to prepare skin homogenate for the detection of CD34 and M30 content with ELISA assay. Results After 30 sessions of treatment with UVA1, the softening and thinning of sclerotic skin were seen by the naked eye, with the most obvious changes in HD-UVA1 group; pathological examination revealed a reduction in dermal thickness and the presence of hair follicular structures in subcutaneous fat tissue with no obvious proliferation of collagen in these mice. Compared with the mice in model control group and unirradiated group, there was an increase in CD34 and decrease in M30 content in skin homogenate from UVA1-irradiated mice, with the most marked changes in mice irradiated with UVA1 at 100 J/cm2. The concentration of CD34 and M30 in skin homogenate from unirradiated group and model control group was significantly different from that in HD-UVA1 group （22.25 ± 8.91 μg/L and 31.97 ± 17.97 μg/L vs. 72.39 ± 13.04 μg/L, 162.41 ± 58.00 U/L and 195.71 ± 71.09 U/L vs. 38.06 ± 19.89 U/L, all P < 0.01）. Additionally, significant differences were observed between the three UVA1 groups in the concentration of CD34 and M30 （F = 21.23, 15.32, respectively, both P < 0.01）. Conclusions UVA1 phototherapy could up-regulate the expression of CD34 but down-regulate that of M30 in skin homogenate from the mouse model of scleroderma, and the effect is correlated with the intensity and cumulative dose of irradiation.

Key words: vascular endothelial cell