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目的 :探讨Ca2 + 及钙调素 (Calmodulin ,CaM )在肺纤维化形成中的作用。方法 :将32只SD大鼠随机分为2组 :(1)正常组 (8只 ) :不接受任何处理。 (2)模型组 (24只 ) :1次性气管内注入博莱霉素A5(BLMA5)制备肺纤维化模型。在实验的第7、14、28d分批处死后作病理切片进行病理学检查 ;应用电子计算机图像分析仪进行肺泡炎和肺间质纤维化定量分析 ;采用火焰原子吸收分光光度法及磷酸二酯酶 (PDE)法分析测定肺组织Ca2 + 含量及CaM活性 ,同时与正常组比较。结果 :模型组肺组织Ca2 +含量及CaM活性较正常组明显增高 (P<0 001) ,组织病理学显示典型的肺间质纤维化病理改变。结论 :BLMA5 诱导的肺纤维化存在着Ca2 + 及CaM平衡紊乱 ,提示Ca2 + -CaM系统在BLMA5 诱导的肺纤维化形成过程中起一定作用
Objective: To investigate the role of Ca2 + and calmodulin (CaM) in the formation of pulmonary fibrosis. Methods: 32 SD rats were randomly divided into two groups: (1) normal group (8): did not receive any treatment. (2) Model group (24 rats): Bleomycin A5 (BLMA5) was infused intratracheally to prepare pulmonary fibrosis model. Pathological examination was performed on the 7th, 14th and 28th day of the experiment in batches. Pathological examination was performed on the pathological sections. The computer image analyzer was used for quantitative analysis of alveolitis and interstitial fibrosis. Flame atomic absorption spectrophotometry and phosphodiester The content of Ca2 + and the activity of CaM in lung tissue were determined by enzyme linked immunosorbent assay (PDE) method and compared with the normal group. Results: The content of Ca2 + and the activity of CaM in lung tissue in model group were significantly higher than those in normal group (P <0.001). Histopathology showed typical pathological changes of pulmonary fibrosis. CONCLUSION: There is a disorder of Ca2 + and CaM balance in pulmonary fibrosis induced by BLMA5, suggesting that Ca2 + -CaM plays a role in BLMA5-induced pulmonary fibrosis