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目的研究UVA对家兔皮肤氧化损伤作用,初步探讨其氧化损伤机制。方法选用成年家兔6只,雌雄各半,采用自身对照的方法将每只家兔分为5个剂量组(0、1、3、5、8 J/cm2)。连续照射染毒7 d后,取家兔皮肤组织进行组织病理学观察和电镜观察,采用免疫组化方法检测家兔皮肤细胞内8-OHdG表达,通过图像分析软件测定图像平均光密度值,并检测皮肤组织匀浆中MDA含量、SOD、GSH-Px活性。结果光镜观察低剂量组表皮层呈修复性增厚、棘细胞增多等现象,随着剂量增大,皮肤组织发生大面积坏死,表皮脱落,真皮层出现毛细血管出血坏死、炎性细胞浸润、细胞核固缩等病理改变。电镜观察真皮成纤维细胞内出现空泡变性,粗面内质网扩张和线粒体损伤,细胞损伤程度随着剂量的增大而加重。除1 J/cm2染毒剂量组外,3 J/cm2,5 J/cm2,8 J/cm2组平均光密度值均高于对照组(P<0.05),且平均光密度值与染毒剂量之间存在良好的剂量-效应关系(r=0.94)。皮肤组织匀浆中的SOD、GSH-Px水平降低,而MDA增加,并存在一定的剂量-效应关系。结论 UVA照射可引起家兔皮肤氧化损伤,其作用机制可能与8-OHdG生成有关。
Objective To study the effect of UVA on skin oxidative damage in rabbits and to explore its mechanism of oxidative damage. Methods Six adult rabbits were randomly divided into five groups (0, 1, 3, 5, 8 J / cm2) by using self-control method. After 7 days of continuous exposure, the skin tissue of rabbits was observed by histopathology and electron microscopy. The expression of 8-OHdG in rabbit skin cells was detected by immunohistochemistry. The average optical density of the images was measured by image analysis software. The content of MDA and SOD, GSH-Px in the skin homogenate were detected. Results In the light microscope, the epidermis of the low-dose group was repaired and thickened, the number of spine cells increased. With the increase of dose, large-scale skin necrosis and epidermis shedding, capillary hemorrhage and necrosis, infiltration of inflammatory cells, Nuclear condensation and other pathological changes. Electron microscopy dermal fibroblasts vacuolar degeneration, rough endoplasmic reticulum dilatation and mitochondrial damage, cell damage increased with increasing dose. The average optical density of 3 J / cm2, 5 J / cm2, 8 J / cm2 group were higher than that of the control group (P <0.05) except 1 J / cm2 dose group, There is a good dose-response relationship (r = 0.94). The level of SOD and GSH-Px in the skin tissue homogenate decreased while MDA increased, and there was a certain dose-effect relationship. Conclusion UVA irradiation can cause skin oxidative damage in rabbits and its mechanism may be related to the formation of 8-OHdG.