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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。
Objective: To investigate the effect of phosphoinositide 3 kinase (PI-3K) on the proliferation of rat airway smooth muscle cells in cigarette smoke-induced chronic obstructive pulmonary disease (COPD). Methods: The model of COPD after cigarette smoke inhalation was established. The airway resistance and respiratory compliance of rats were measured. HE staining and PCNA immunohistochemistry were performed on airway smooth muscle. Reverse transcription-polymerase chain reaction (RT- PCR) to detect the expression of PI-3K mRNA in airway smooth muscle. Results: The airway resistance was increased in COPD group (P <0.05). The expression of PCNA and PI-3K mRNA in airway smooth muscle of COPD group was significantly higher than that of control group (P <0.05) The expression of PI-3K mRNA was positively correlated with the expression of PCNA (r = 0.856, P <0.05). Conclusion: Cigarette smoke may play a role in the proliferation of airway smooth muscle cells in COPD rats through the PI-3K signaling pathway.