大鼠哮喘模型气道重塑中细胞增殖和凋亡的变化

Changes of cell proliferation and apoptosis in airway remodeling of experimental asthmatic rats

目的 :探讨大鼠哮喘气道重塑中细胞增殖和凋亡的变化 ,以及地塞米松对其影响。方法 :将 39只大鼠随机等分为正常对照组、哮喘模型组和地塞米松干预组 ,以卵蛋白致敏制作大鼠哮喘模型 ,病理观察 3组气道壁形态学改变 ;采用免疫组化方法观察细胞增殖核抗原 (PCNA)和Caspase 3在气道壁和肺组织中的表达。结果 :哮喘模型组气道壁、气道周围及肺泡区细胞PCNA阳性表达 (1 3.0 0± 1 .87,2 0 .4 6± 4 .1 6 )明显高于正常对照组的 (1 0 .0 0± 2 .2 0 )及 (1 5 .0 0± 4 .83) (P <0 .0 5 ) ,且与气道上皮层、黏膜层厚度及胶原沉积面积呈正相关 (r=0 .6 7,0 .6 6 ,0 .5 7;P <0 .0 5 )。地塞米松干预组PCNA表达 (9.5 4± 2 .1 5 ,1 3.0 8± 3.4 0 )明显低于哮喘模型组 ,Caspase 3表达 (5 .38± 1 .4 5 ,3.82± 1 .70 )高于哮喘模型组 (4 .92± 1 ,85 ,5 .6 2± 1 .5 6 ) (P <0 .0 5 )。结论 :细胞增殖过度和凋亡异常是哮喘气道炎症和重塑反应的重要机制之一 。

Aim:To explore the change of cell proliferatation and apoptosis in airway remodeling of asthmatic rats and the effect of dexamesone. Methods: SD rat were divided into normal group,model group and dexamesone group.Asthmatic rat models were established by repeated ovalbumin sensition. The morphological changes of airway were observed; the expression of PCNA and Caspase 3 was estimated by immunohistochemical technique. Results: The expression of PCNA in model group were higher than those of normal and dexamesone groups,and positive correlated with the depth of airway epithelia and mucosa layers and collagen deposit area. The expression of Caspase 3 in dexamesone group was higher than that of model group. Conclusion:The disorder of cell proliferation and apoptosis is one of the important mechanisms of airway inflammation and remodeling in asthma, and dexamesone can prevent airway remodeling by regulating the cell proliferation and apoptosis.