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目的探讨P27Kip-1对哮喘大鼠气道平滑肌细胞增生及气道重塑的影响。方法清洁级雄性SD大鼠30只,随机分成对照组(C)、哮喘4周组(A1)、哮喘6周组(A2)每组10只。用卵白蛋白(OVA)致敏与激发建立大鼠哮喘模型,末次激发后24h内测气道反应性和观察气道壁炎性细胞的浸润情况,图像分析软件测定支气管壁厚度、支气管平滑肌厚度;免疫组化法检测增生细胞核抗原(PCNA)及P27Kip-1表达。结果哮喘4周和6周组P27Kip-1蛋白表达显著低于对照组(P<0.05),且6周组低于4周组(P<0.05);哮喘4周和6周组PCNA表达、支气管壁厚度、支气管平滑肌厚度和气道反应性均显著高于对照组(P<0.01),且6周组高于4周组(P<0.01)。结论P27Kip-1可抑制气道平滑肌细胞增生进而影响气道重构与气道高反应性。
Objective To investigate the effect of P27Kip-1 on airway smooth muscle cell proliferation and airway remodeling in asthmatic rats. Methods Thirty male SD rats were randomly divided into control group (C), asthma group of 4 weeks (A1), asthma group of 6 weeks (A2) of 10 rats. The model of asthma was established by ovalbumin (OVA) sensitization and challenge. The airway responsiveness and the infiltration of inflammatory cells were observed 24h after the last challenge. The thickness of bronchial wall and bronchial smooth muscle were measured by image analysis software. Immunohistochemistry was used to detect the expression of proliferating cell nuclear antigen (PCNA) and P27Kip-1. Results The expression of P27Kip-1 protein at 4 and 6 weeks after asthma in asthma group was significantly lower than that in control group (P <0.05), and was lower in 6 weeks than in 4 weeks group (P <0.05) Wall thickness, bronchial smooth muscle thickness and airway reactivity were significantly higher than those in the control group (P <0.01), and were higher in the 6-week group than in the 4-week group (P <0.01). Conclusion P27Kip-1 can inhibit airway smooth muscle cell proliferation and thus airway remodeling and airway hyperresponsiveness.