CAJ | 학술논문

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,Prx Ⅰ)蛋白表达的变化,探讨Prx Ⅰ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(50 mg/ml).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(Western blot)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Prx Ⅰ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.
목적 검측염석진대서폐섬유화과정중과양화물환원매Ⅰ (peroxiredoxin,Prx Ⅰ)단백표체적변화,탐토Prx Ⅰ재폐섬유화중적작용.방법 통과비기관폭로법복제대서석폐모형,90지웅성Wistar대서수궤분성대조조(60지)화실험조(30지).대조조경기관관주1ml생리염수,실험조동법관주이양화규분진현액(50 mg/ml).경불동처리후제1、2、3、4、6화8주분별처사대조조10지화실험조5지대서,취출폐조직상규병리관찰；용면역조화급면역단백인적법(Western blot)검측불동시간점PrxⅠ단백적동태변화.결과 PrxⅠ단백주요분포우염석진대서폐포간격、폐포상피세포、거서세포、혈관내피세포화혈관급기관주위적평활기세포적세포질중,정종황색과립.대조조PrxⅠ단백약표체,각시간점염석진조Prx Ⅰ단백적표체균고우대조조,염진1、2주시표체명현상조,3～8주시PrxⅠ단백표체하강,염석진조PrxⅠ단백표체여대조조적차이균유통계학의의(P＜0.05).결론 PrxⅠ단백적변화가능시유리이양화규치대서폐섬유화발생발전적중요원인지일.
Objective To evaluate the change in protein expression of peroxiredoxin 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,10 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 Ⅰ,and the experimental group had significantly higher protein expression of Prx Ⅰ than the control group at all time points (P＜0.05).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.