咳喘宁对支气管哮喘大鼠肺组织嗜酸粒细胞凋亡及调控基因表达的影响

目的观察咳喘宁对支气管哮喘大鼠肺组织嗜酸粒细胞凋亡及调控基因Bcl-2、Bax表达的影响。方法40只SD大鼠随机分为正常组、模型组、咳喘宁高剂量组（27．0g生药／kg体重）、咳喘宁低剂量组（13．5g生药／kg体重）、桂龙咳喘宁对照组（0．41g／kg体重），每组8只。除正常组外，以卵蛋白致敏并吸入激发法制备大鼠支气管哮喘模型，各治疗组均从第1次哮喘激发开始（造模第3周）至处死前每日灌胃给药，激发并给药4周后处死大鼠，采用TUNEL法检测细胞凋亡，免疫组化检测凋控基因Bcl-2、Bax表达，采用HE染色观察肺和气管病理组织学变化。结果与正常组比较，模型组大鼠支气管管壁和平滑肌厚度、嗜酸粒细胞、淋巴细胞数以及肺组织Bcl-2表达的细胞比例明显增加，Bax表达的细胞比例显著降低；与模型组比较，各治疗组均可显著降低支气管管壁和平滑肌厚度、嗜酸粒细胞、淋巴细胞数以及Bcl-2阳性细胞的比例，升高Bax表达阳性细胞比例和嗜酸粒细胞凋亡指数。结论咳喘宁通过调节凋亡基因表达，促进嗜酸粒细胞凋亡，减轻哮喘气道炎症。

Effect of Kechuanning on the Apoptotic and Controlling Gene Expression Of EOS in Lung Tissue of Bronchial Asthmatic Rats

Objective： To observe effect of Kechuanning on the apoptotic and controlling gene Bcl - 2, Bax expression of EOS in lung tissue of bronchial asthmatic rats. Methods： 40 rats were randomly divided into 5 groups： the normal group, the model group, Kechuanning high -dose group（27g/kg）, Kechuanning low -dose group（13.5g/ kg）, Guilongkechuanning control group （0.45g/kg）, 8 rats in each group. The bronchial asthmatic model was established by egg protein sensibilization and long - term inhalation provocation. The rats of each treatment groups were lavage administration each day from the first time of provocation to execution. After 4 weeks of treatment, the rats were killed and lung tissue were taken to dyeing of HE to be observed. The apoptotic of EOS in lung tissue were determined by TUNEL. The expression of Bcl - 2, Bax in lung tissue were determined by immunohistochemistry. Results： Compared with the normal group, the thickness of bronchus wall and bronchus smooth muscle, the numbers of eosinophile granulocyte and leukomonocyte, and expression of Bcl - 2 in lung tissue were increased and expression of Bcl - 2 were decreased in the model group; Compared with the model group, the thickness of bronchus wall and bronchus smooth muscle, the numbers of eosinophile granulocyte and leukomonocyte, the expression of Bcl - 2 in lung tissue were decreased, and the expression of Bax and apoptotic numbers were increased in each treatment group. Conclusion： Kechuanning can regulate apoptotic genetic expression to increase EOS apoptotic and restrain air passage inflammation.