中文摘要：

目的：探讨雷公藤内酯醇对哮喘气道重构及核因子-kappaB（NF-κB）、Bcl-2表达的影响。方法：将40只SD大鼠随机分为5组（n=8）：正常对照组（A组）;哮喘4周组（B组）;哮喘6周组（C组）;治疗4周组（D组）;治疗6周组（E组）。测定气道反应性并观察气道壁嗜酸性粒细胞浸润;图像分析软件测定支气管壁厚度、支气管平滑肌厚度及支气管平滑肌细胞核数量;免疫组织化学染色、Western印迹法检测PCNA、NF-κB、Bcl-2蛋白的表达,逆转录聚合酶链式反应（RT-PCR）检测Bcl-2mRNA表达。结果：①B组、C组NF-κB的蛋白表达量显著高于A组（P均〈0.01）,E组上述指标较B组、C组、D组均显著降低（P〈0.01、P〈0.01、P〈0.05）;②B组、C组Bcl-2蛋白及mRNA表达水平显著高于A组（P〈0.01）;E组蛋白表达量较B组、C组、D周组均显著降低（依次为P〈0.05、P〈0.01、P〈0.01）,mRNA表达水平与上述各组比较亦均显著降低（P〈0.01）,E组蛋白及mRNA表达水平与A组相比仍较高（依次为P〈0.05、P〈0.01）;③B组、C组PCNA的蛋白表达量明显高于A组（P〈0.01）;④B组及C组支气管壁厚度、支气管壁平滑肌厚度、支气管壁平滑肌细胞核数量均较A组明显增加（P〈0.01）,而E组上述指标较B组、C组、D组均显著降低（P〈0.01）;⑤B组、C组的气道反应性均高于A组（P均〈0.01）,E组较B组、C组、D组均显著降低（P〈0.01、P〈0.01、P〈0.05）。结论：哮喘气道平滑肌增生与气道平滑肌细胞（ASMCs）凋亡不足相关。NF-κB可能通过抑制ASMCs凋亡,参与哮喘气道高反应性及气道重构过程。雷公藤内酯醇可能通过下调NF-κB而抑制Bcl-2的表达,从而促进ASMCs凋亡、抑制气道平滑肌增生。

英文摘要：

Objective：To explore the effect of triptolide on airway remodeling and the expression of nuclear factor-κB,Bcl-2 in asthmatic rats. Methods： 40 rats were randomly divided into 5 groups （n=8）： ①Control group; ②Asthmatic 4 week group; ③Asthmatic 6 week group; ④Therapeutic 4 week group; ⑤Therapeutic 6 week group. The airway resistance and eosinophilic inflammation of airway wall were observed. The airway wall thickness （WA/Pi）,the bronchial smooth muscle thickness （smooth muscle area/Pi） and the number of bronchial smooth muscle nucleus （N/Pi） were measured by image analysis system. The expression of PCNA,nuclear factor-κB and Bcl-2 protein were determined by immunohistochemical staining and Western blot. The expression of Bcl-2 mRNA was determined by reverse transcription-polymerase chain reaction（RT-PCR）. Results： ① The expression of NF-κB protein in asthmatic 4 week group and asthmatic 6 week group was significantly higher than that in control group,respectively（P0.01）. The above-mentioned parameters of therapeutic 6 week group were significantly lower than those of asthmatic 4 week group,asthmatic 6 week group and therapeutic 4 week group,respectively （P0.01,P0.01 P0.05）. ②The expression of Bcl-2 protein and mRNA of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those in control group respectively（P0.01）. The expression of Bcl-2 protein of therapeutic 6 week group was significantly lower than those of asthmatic 4 week group,asthmatic 6 week group and therapeutic 4 week group respectively （P0.05,P0.01,P0.01）,but the expression of Bcl-2 mRNA was significantly higher than the above-mentioned groups respectively （P0.01）,the expression of Bcl-2 protein and mRNA of therapeutic 6 week group were higher than control group respectively （P0.05,P0.01）.③The expression of PCNA protein of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those of control group respectively （P0.01）. ④The