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目的:观察博莱霉素所致肺纤维化大鼠微血管内皮细胞(LMVECs)超微结构及血清CTGF的变化,探讨肺微血管内皮细胞表型及与博莱霉素损伤肺纤维化间的关系.方法:SD大鼠45只,随机分为3组:博莱霉素(BLM)组,肺炎链球菌组及正常对照组,每组15只,分别气管滴注博莱霉素及肺炎链球菌造模,对照组滴注生理盐水.电镜观察外周肺组织内皮细胞超微结构,同时测定血清CTGF含量.结果:光镜及电镜显示肺炎组与BLM组的不同改变.肺炎组组织学及肺微血管内皮细胞超微结构表现为典型的急性炎症损伤修复,之后肺组织结构恢复正常.BLM组表现为肺组织损伤的持续进行,肺微血管内皮细胞7d开始增殖并出现形态学的改变,且贯穿实验各个阶段,最终胶原明显沉积于肺泡间隔.血清CTGF测定:肺炎组3d开始增高,第7d骤降至(5.04±0.82)ng/L,第21d恢复至(12.06±0.43)ng/L.BLM组全程增高,第7d至(12.53±2.36)ng/L,第21d增至高峰(19.45±0.41)ng/L.结论:肺微血管内皮细胞功能的转变及其分泌CTGF时相和量的异常可能是博莱霉素所致肺纤维化发生发展的重要环节.
OBJECTIVE: To observe the ultrastructural changes of the microvascular endothelial cells (LMVECs) and serum CTGF in pulmonary fibrosis rats induced by bleomycin, and to explore the relationship between the phenotype of pulmonary microvascular endothelial cells and bleomycin-induced pulmonary fibrosis. Methods: Forty-five SD rats were randomly divided into three groups: bleomycin (BLM) group, Streptococcus pneumoniae group and normal control group, with 15 rats in each group. Bleomycin and Streptococcus pneumoniae were respectively intratracheally instilled The model group and the control group were given normal saline.Electron microscope was used to observe the ultrastructure of the endothelial cells in the peripheral lung tissue and to determine the content of CTGF in the serum.Results: The changes of pneumonia group and BLM group were observed by light microscopy and electron microscope.The histological and pulmonary microvascular endothelial The ultrastructure of the cells showed typical acute inflammatory injury repair, and then the lung tissue structure returned to normal.BLM group showed the continuous lung injury, pulmonary microvascular endothelial cells began to proliferate 7d and morphological changes, and throughout all stages of the experiment , The final collagen was obviously deposited in the alveolar septum.Serum CTGF assay: The pneumonia group began to increase at 3d, dropped to (5.04 ± 0.82) ng / L on the 7th day and returned to (12.06 ± 0.43) ng / L. on the 21st day , From the 7th day to (12.53 ± 2.36) ng / L, the second day 1d to peak (19.45 ± 0.41) ng / L. CONCLUSION: Functional changes of pulmonary microvascular endothelial cells and the abnormality of phase and amount of CTGF secretion may be an important link in the development of bleomycin-induced pulmonary fibrosis.