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目的研究高体积分数氧(高氧)肺损伤早产鼠肺组织小窝蛋白-1的动态表达及其与肺纤维化的关系。方法剖宫术取出孕21 d大鼠作为早产鼠,30只新生早产W istar大鼠生后12 h随机分为高氧组和对照组,每组15只,高氧组持续暴露于950 mL.L-1氧气中,空气组置于同一室内常压空气中。分别于暴露1 d、3 d、7 d时,每组取动物5只,留取其肺组织标本,常规制成5μm切片,应用HE染色观察不同时间点其肺组织病理改变,在光镜下进行肺组织纤维化评分,并采用免疫组织化学法检测不同时间点其肺组织小窝蛋白-1的表达部位和强度,将小窝蛋白-1的表达与肺纤维化进行相关性分析。结果早产鼠高氧暴露3 d后出现明显急性炎症改变,肺泡内有出血和炎性细胞浸润,间质纤维化,且病变随高氧暴露时间的延长而加重;小窝蛋白-1在对照组早产大鼠肺组织中均有较高水平表达,高氧组早产鼠吸入高氧1 d,肺组织小窝表达出现降低,在3 d、7 d明显降低,与对照组比较差异均有统计学意义(Pa<0.05),尤以高氧7 d最明显;小窝蛋白-1与纤维化评分呈负相关(Pa<0.05)。结论高氧诱导急性肺损伤,导致早产鼠肺组织小窝蛋白-1表达持续性减少,其异常表达可能是导致肺成纤维细胞过度增殖,最终发生肺间质纤维化的重要原因。实用儿科临床杂志,2011,26(12):959-961
Objective To investigate the dynamic changes of lung tissue protein-1 expression and its relationship with pulmonary fibrosis in premature rats with high volume fraction of oxygen (hyperoxia) lung injury. Methods Cesarean section was taken as premature pregnancy in 21 d pregnant rats. Thirty newborn preterm Wistar rats were randomly divided into hyperoxia group and control group at 12 h after birth. The rats in each group were exposed to 950 mL of hyperoxia group. L-1 oxygen, the air group placed in the same room atmospheric air. The animals were sacrificed on day 1, day 3 and day 7, respectively. Five animals in each group were taken from the lungs and their lung tissues were collected. The sections were routinely made into 5μm sections. The pathological changes of lungs were observed at different time points by HE staining. Lung fibrosis was scored and immunohistochemistry was used to detect the expression site and intensity of caveolin-1 in lung tissue at different time points. The correlation between caveolin-1 expression and pulmonary fibrosis was analyzed. Results In premature rats exposed to hyperoxia for 3 days, there were obvious changes of acute inflammation, hemorrhage and infiltration of inflammatory cells in the alveoli, interstitial fibrosis, and the pathological changes were aggravated with the prolongation of hyperoxia exposure. In the control group Premature rats lung tissue were higher levels of expression, hyperoxia group premature rats inhaled hyperoxia 1 d, lung tissue expression decreased, in the 3 d, 7 d significantly reduced compared with the control group were statistically significant (P <0.05), especially at 7 days of hyperoxia. The expression of caveolin-1 was negatively correlated with fibrosis score (Pa <0.05). Conclusions Hyperoxia-induced acute lung injury leads to the persistent decrease of the expression of caveolin-1 in premature rats. Abnormal expression may be the important reason for the excessive proliferation of pulmonary fibroblasts and eventually pulmonary fibrosis. Practical Journal of Pediatrics, 2011,26 (12): 959-961