【摘要】 目的:探讨香烟烟雾吸入诱导的慢性阻塞性肺疾病(COPD)中磷酰肌醇3激酶(PI-3K)对大鼠气道平滑肌细胞增殖的影响。方法:制作大鼠吸入香烟烟雾后的COPD模型,测定大鼠气道阻力及呼吸系统总顺应性,对气道平滑肌进行HE染色及PCNA免疫组化观察,并且逆转录聚合酶链反应(RT-PCR)检测气道平滑肌中PI-3KmRNA的表达。结果:COPD组呼吸功能检查显示气道阻力增加(P<0.05);COPD组气道平滑肌在PCNA免疫组化及PI-3K mRNA表达与对照组相比有显著性增高(P<0.05),而且PI-3K mRNA的表达水平与PCNA的表达水平的呈明显正相关(r=0.856,P<0.05)。结论:香烟烟雾可能通过PI-3K信号途径在COPD大鼠气道平滑肌细胞增殖中发挥作用。更多还原

【Abstract】 Objective: To study the effect of the phosphoinositide 3 kinase(PI-3K) expression on the proliferation of airway smooth muscle cells(ASMCs) in rats with chronic obstructive pulmonary disease(COPD) induced by smoking.Methods: The rat models of COPD induced by smoking were made to investigate the resistance of airway and the total compliance of respiratory system.The expression of PCNA in ASMCs was determined by immunohistochemistry,and the mRNA expression of PI-3K in ASMCs was determined by reverse transcription polymerase chain reaction(RT-PCR).Results: The resistance of airway was increased in the COPD groups as compared with control group,and the expressions of PCNA and PI-3K in ASMCs of COPD groups were significantly increased(all P<0.05,n=15).The expression level of PI-3K had strongly positive correlation with the expression level of PCNA(r=0.856,P<0.05,n=15).Conclusion: The PI-3K signal pathway may be involved in ASMCs proliferation in COPD rats induced by smoking.更多还原