中文摘要：

目的探讨Sonic hedgehog信号通路中Smo和Gli1蛋白在高氧诱导的急性肺损伤中的表达及意义。方法通过持续吸入高浓度氧气建立新生大鼠高氧肺损伤模型。实验组吸入95%的医用氧气,对照组吸入空气。分别留取第3、7和14 d的肺组织,HE染色观察肺脏病理改变,应用免疫组织化学和Western blot检测肺组织中Smo和Gli1蛋白的动态表达情况。结果高氧暴露3 d肺毛细血管开始充血、渗出;7 d时肺结构紊乱,炎性细胞浸润;14 d时肺泡融合,纤维增生,间隔增宽。高氧组Smo和Gli1蛋白主要分布于支气管上皮、肺泡上皮、血管内皮细胞及部分纤维组织。与对照组相比,Smo于高氧第7天表达显著增加,第14天达高峰;Gli1蛋白表达于14 d显著增加。结论高浓度氧可致新生大鼠肺损伤和肺发育停滞。Smo和Gli1蛋白的高表达可能与高氧诱导的肺损伤和支气管肺发育不良的发生发展有关。

英文摘要：

Objective To investigate the expressions of Smo and Glil signaling molecules in lungs of newborn rats exposed to prolonged hyperoxia, and to explore the role of sonic hedgehog （SHH） signaling pathway in hypemxia-induced lung injury. Methods Neonatal rat pups were placed in chambers containing room air or 95% medical oxygen for 14 days after birth. Then the rats were sacrificed at 3,7 and 14 days and their lungs were removed and subjected to hematoxylin and eosin（HE） staining. The dynamic expressions of Smo and Glil proteins were observed by immunohistochemistry and Western blot. Results Significant histo-morphologic changes were found in the hyper- oxia-exposed lungs at 3,7 and 14 days by HE staining. Smo and Glil proteins were observed in bmnchial epithelial cells,alveolar epithelial cells, and vascular endothelium cells, and partly showed on the fibrotic tissues in lung interstitium. The results of immunohistochemistry and the Western blot showed that the expression of Smo protein was significantly higher in the hyperoxia-exposed lungs at 7 and 14 days, and Glil expression was significantly elevated at 14 days. And low Smo and Glil were detected in normal air group. Conclusion Exposure of neonatal rats to prolonged hyperexia results in acute lung injury and arrested lung development. Smo and Glil are up-regulated at time points preceding the lung injury,and SHH signal pathway seems to be involved in the pathogenesis of hyperoxia-induced lung injury and bron- ehopulmonary dysplasia.