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目的探讨高氧诱导新生大鼠急性肺损伤中Shh信号通路Smo和Gli1蛋白的表达及其意义。方法建立早产新生大鼠高氧肺损伤模型。实验组持续吸入氧体积分数大于95%的医用氧气,对照组吸入空气。分别留取第3、7、14天的肺组织,肺组织切片HE染色观察肺脏病理改变,应用Western blot技术检测肺组织Smo和Gli1蛋白的动态表达情况。结果实验组高氧暴露3天肺毛细血管开始充血、渗出;7天肺结构紊乱,炎性细胞浸润;14天肺泡融合,纤维增生,间隔增宽。实验组Smo和Gli1蛋白主要分布于支气管上皮、肺泡上皮细胞、血管内皮细胞及部分纤维组织。与对照组相比,实验组高氧第7天Smo蛋白表达显著增加[(0.423±0.056)比(0.061±0.008)],14天达高峰[(0.612±0.082)比(0.132±0.011)];Gli1蛋白于14天表达显著增加[(0.515±0.071)比(0.209±0.013)],P均<0.05。结论高氧可致新生大鼠肺泡结构紊乱和肺发育停滞,Smo和Gli1蛋白呈现高表达,这可能和高氧诱导的肺损伤和支气管肺发育不良的发生发展有关。
Objective To investigate the expression and significance of Shh signaling pathway Smo and Gli1 in neonatal rats with hyperoxia-induced acute lung injury. Methods The model of hyperoxic lung injury in premature neonatal rats was established. The experimental group continued to inhale medical oxygen with the volume fraction of oxygen greater than 95%, while the control group inhaled air. Lung tissues were collected on the 3rd, 7th and 14th days respectively. The pathological changes of the lungs were observed by HE staining and the expression of Smo and Gli1 protein in lung tissues were detected by Western blot. Results In the experimental group, the pulmonary capillaries began to hyperemia and exudation 3 days after exposure to hyperoxia. The lungs were disorganized and infiltrated by inflammatory cells for 7 days. The alveolar fusion and fibrogenesis were broadened after 14 days. The experimental group Smo and Gli1 protein mainly in bronchial epithelial cells, alveolar epithelial cells, vascular endothelial cells and some fibrous tissue. Compared with the control group, the expression of Smo protein in the experimental group increased significantly (P <0.05) on the 7th day [(0.423 ± 0.056) vs (0.061 ± 0.008)] and reached the peak on the 14th day (0.612 ± 0.082 vs 0.132 ± 0.011) The expression of Gli1 protein increased significantly on day 14 [(0.515 ± 0.071) vs (0.209 ± 0.013)], P <0.05. Conclusions Hyperbaric oxygen can cause the disturbance of alveolar structure and pulmonary development in neonatal rats, and the high expression of Smo and Gli1 protein, which may be related to the development of hyperoxia-induced lung injury and bronchopulmonary dysplasia.