摘要
目的探讨高浓度氧对新生鼠肺组织血管内皮生长因子(VEGF)蛋白表达及肺血管内皮细胞超微结构影响的动态变化规律。方法建立高浓度氧诱导新生鼠CLD模型,60只新生鼠随机分为实验组和对照组,分别采用免疫组化和透射电镜技术,测定实验组和对照组在生后1d、3d、7d、14d和21dl肺组织内VEGF蛋白表达,同时观察肺血管内皮细胞超微结构变化。结果对照组肺组织VEGF蛋白表达1d主要以传导气道上皮为主,3d以后远端气道上皮表达增加,7d以后肺泡上皮和肺泡间隔明显增多,14d达高峰,以后持续高表达,实验组肺组织VEGF蛋白表达水平7d开始下降,14d以后未见阳性表达。高氧可引起肺血管内皮细胞肿胀、线粒体肿胀和毛细血管基底膜厚薄不均等各种损伤性形态变化,损伤程度随高氧时间延长而加重。结论肺血管的生长是正常肺泡发育重要环节,推测肺组织VEGF蛋白表达下降和肺血管内皮细胞的损伤在高氧诱导CLD肺血管发育障碍中可能发挥重要作用。
Objective :To explore the dynamic changes of the expression of VEGF protein in the lung and uhrastructure of pulmonary vascular endothelial cell in neonatal rats with hyperoxia. Methods :Sixty neonatal rats were randomly divided into 2 group( n = 30) : experimental group with CLD induced by hyperoxia, and control group. The expression of VEGF protein in the lung was determined by using immunohistochemical methods. We observed the changes of ultrastructure of pulmonary vascular endothelial cell by using TEM. Results :The VEGF protein was mainly expressed in the epithelium of the conductive airway on the 1 day and gradually increased in distant epithelial cells after the 3th day in the control group. But in the experimental group with CLD induced by hyperoxia,the expression level of VEGF protein was very lower than that of the control group on the 7th day and to the lowest level on days 14;It was hardly to see the VEGF positive cells on 14d,21d;There was no signifieient difference between the two group.on ld,3d P 〉0, 05 ,but on 7d, 14d,21d, P 〈 0. 01. In the experimental group, changes of ultrastructure of pulmonary capillary endothelial cell was Characterized by endothelial cell and mitochondria swellest, capillary basement membrane unequal. Conclusion:Between decreased expression of VEGF protein and the injuries of pulmonary capillary endothelial cell might play an important role in the developmeht of pulmonary vascular dysplasia in hyperoxia -induced chronic lung disease.
出处
《中国优生与遗传杂志》
2006年第2期20-21,19,F0004,共4页
Chinese Journal of Birth Health & Heredity
关键词
血管内皮生长因子
慢性肺疾病
超微结构
Vascular endothelial growth factor
Chronic lung disease
Ultrastructure