染矽尘大鼠肺组织过氧化物还原酶I蛋白表达的变化  

Expression of peroxiredoxin I in the rats exposed to silica

作　　者：郑素琴[1] 桑银洲[1] 孙影[1] 张宏伟 熊艳杰 伊雪[1] 王俊然[3] 

机构地区：[1]河北联合大学基础医学院病理学系,唐山063000 [2]附属医院病理科 [3]唐山市妇幼保健院病理科

出　　处：《中华劳动卫生职业病杂志》2013年第7期531-533,共3页Chinese Journal of Industrial Hygiene and Occupational Diseases

基　　金：河北省科学技术研究与发展计划项目（10276114D）

摘　　要：目的检测染矽尘大鼠肺纤维化过程中过氧化物还原酶I（peroxiredoxin，PrxI）蛋白表达的变化，探讨PrxI在肺纤维化中的作用。方法通过非气管暴露法复制大鼠矽肺模型，90只雄性Wistar大鼠随机分成对照组（60只）和实验组（30只）。对照组经气管灌注1ml生理盐水，实验组同法灌注二氧化硅粉尘悬液（50mg／m1）。经不同处理后第1、2、3、4、6和8周分别处死对照组10只和实验组5只大鼠，取出肺组织常规病理观察；用免疫组化及免疫蛋白印迹法（Westernblot）检测不同时间点PrxI蛋白的动态变化。结果PrxI蛋白主要分布于染矽尘大鼠肺泡间隔、肺泡上皮细胞、巨噬细胞、血管内皮细胞和血管及气管周围的平滑肌细胞的细胞质中，呈棕黄色颗粒。对照组PrxI蛋白弱表达，各时间点染矽尘组PrxI蛋白的表达均高于对照组，染尘1、2周时表达明显上调，3-8周时PrxI蛋白表达下降，染矽尘组PrxI蛋白表达与对照组的差异均有统计学意义（p〈0．05）。结论PrxI蛋白的变化可能是游离二氧化硅致大鼠肺纤维化发生发展的重要原因之一。Objective To evaluate the change in protein expression ofperoxiredoxin I （Prx I） during pulmonary fibrosis among rats exposed to silica dust and to investigate the role of Prx I in pulmonary fibrosis. Methods Ninety male Wistar rats were randomly divided into control group （n=60） and experimental group （n=30）. The control group received intratracheal perfusion of saline （1 ml）, while the experimental group received intratracheal perfusion of suspension of silica dust （50 mg/ml） to establish a rat model of silicosis. At 1, 2, 3, 4, 6, or 8 weeks after treatment, l0 rats in control group and 5 rats in experimental group were sacrificed. The lung tissues were collected for conventional pathological observation. The protein expression of Prx I at each time point was measured by immunohistochemistry and Western blot. Results Among the rats exposed to silica dust, Prx I was seen in the form of brown particles that were mainly distributed in the alveolar septa and the cytoplasm of alveolar epithelial cells, macrophages, vascular endothelial cells, and smooth muscle cells around the blood vessels and tracheae. The control group showed weak protein expression of Prx 1, and the experimental group had significantly higher protein expression of Prx I than the control group at all time points （P〈O.05）. In the experimental group, the protein expression of Prx I was upregulated significantly at 1 and 2 weeks and decreased at 3-8 weeks. Conclusion The change in protein expression of Prx I may be one of the important causes of the onset and development of pulmonary fibrosis in rats exposed to free silica.

关 键 词：二氧化硅 肺纤维化 过氧化物酶类 

分 类 号：R135.2[医药卫生—劳动卫生]