目的 探讨硫氧环蛋白过氧化物酶1（Prx-1）对硅沉着病小鼠肺功能的影响。  方法 C57BL/6小鼠随机分为对照组（生理盐水）、硅沉着病组（SiO2）、阴性转染组（SiO2+慢病毒空载体）和Prx-1转染组（SiO2+慢病毒Prx-1过表达载体），每组10只。气管插管术辅以呼吸机一次性灌注SiO2悬液和慢病毒载体。模型制备后，小鼠常规饲养12周。HE染色观察肺组织形态变化，免疫组织化学法检测8-羟基脱氧鸟苷(8-OhdG) 表达，Western blotting法检测肺组织Prx-1、Ⅰ和Ⅲ型胶原水平，FinePointe WBP 全身体积描记系统检测肺功能。  结果 对照组小鼠肺组织结构基本正常，硅沉着病组和阴性转染组中可见矽结节形成，Ⅰ和Ⅲ型胶原表达增多，Prx-1转染组肺组织病变减轻，矽结节变小，Ⅰ和Ⅲ型胶原水平降低。与对照组比较，硅沉着病组和阴性转染组8-OHdG水平及Prx-1蛋白表明显增加，但Prx-1转染组的8-OHdG水平较硅沉着病组减少，Prx-1表达较硅沉着病组增加。与对照组比较，硅沉着病组和阴性转染组小鼠肺功能降低，但Prx-1转染组小鼠肺功能明显改善。  结论 Prx-1高表达可通过降低活性氧，抑制硅沉着病纤维化和改善肺功能。

Objective To investigate the effect of peroxiredoxin-1 (Prx-1) on pulmonary function induced by silicosis. Methods Forty C57BL/6 mice were randomly divided into control group (normal saline), silicosis group (SiO2), negative control group (SiO2+empty lentivirus) and Prx-1 group (SiO2+Prx1 lentivirus). Crystalline silica instillation and lentivirus were given via trachea, and then all mice were normally raised for 12 weeks. HE staining was used to observe the morphological changes of lung tissue. The expressions of 8-hydroxy-2 deoxyguanosine (8-OHdG), Prx-1, collagen type Ⅰ and Ⅲ were detected by immunohistochemistry and Western blotting respectively. FinePointe WBP whole body plethysmography system was employed to measure the pumonary function.   Results It had the normal structure of lung tissue in control group. SiO2 markedly induced silicosis formation and increase in collagen typeⅠ and Ⅲ, with a similar extent of silicotic nodules and collagen expression in silicosis group and negatively control group, but Prx-1 lentivirus treatment ameliorated these pathological changes. SiO2 increased 8-OHdG and Prx-1 expressions significantly. There were no changes between silicosis group and negative control group. But the level of 8-OHdG in Prx-1 group was lower than silicosis group and Prx-1 level was higher than silicosis group. SiO2 also decreased the pulmonary function significantly. Compared with silicosis group, the mice lung function was improved in Prx-1 group, but there was no effect of empty lentivirus transfection.   Conclusion Overexpression of Prx-1, mediated by decrease in reactive oxygen species(ROS), improves the pulmonary function in mice with silicosis.