布地奈德对哮喘大鼠支气管-肺组织病理及肺部TSLP表达的影响

Effects of inhaled budesonide on the bronchial-pulmonary pathology and expression of thymic stromal lymphopoietin in lung tissues in asthmatic rats

目的胸腺基质淋巴细胞生成素(thymic stromal lymphopoietin,TSLP)是启动树突状细胞介导的过敏反应的重要物质。本研究旨在观察布地奈德对哮喘大鼠肺部TSLP表达的影响及对支气管-肺组织病理的影响。方法采用卵清蛋白(OVA)腹腔注射2次致敏及雾化吸入4周激发建立哮喘大鼠模型,并在激发第22天将动物随机分为布地奈德组(每天吸入布地奈德0.32mg/kg,共7d)、哮喘组(每天吸入等量生理盐水,共7d)。荧光免疫组化法、Western blot法分别检测激发后第29天、36天肺TSLP水平,并作支气管-肺组织病理检查。结果布地奈德组第29天肺部炎症较哮喘组轻,停药7d后肺部炎症明显加重,杯状细胞增多。激发后第29天、36天肺组织TSLP表达均低于哮喘组(P<0.05)。结论布地奈德能抑制TSLP表达,减轻哮喘大鼠肺部炎症细胞浸润,但停药后肺部炎症再次加重。

Objective Thymic stromal lymphopoietin （TSLP） plays an important role in initiating dendritic cell mediated allergic inflammation. This study was designed to examine the effects of inhaled budesonide on TSLP expression in the lung tissues and on the bronchial-pulmonary pathology in asthmatic rats. Methods Thirty-two female Sprague- Dawley rats were sensitized and challenged with inhaled ovabumin （ OVA） to induce asthma. The asthmatic rats were randomly divided into 2 groups on the 22nd day of OVA challenge： a budesonide treatment group that received inhaled budesonide at 0. 32 mg /kg daily for 7 days and an asthma control group that received inhaled 0. 9% normal saline for 7 days. TSLP expression in the lung tissues was measured by Western blot and fluorescent-immunohistochemistry 29 and 36 days after OVA challenge. Bronchial-pulmonary pathological changes were evaluated by hematoxylin eosin and periodic acid-schiff staining. Results Budesonide treatment alleviated airway inflammation when compared with the asthma control group 29 days after OVA challenge. However,the airway inflammatory reactions were aggravated in the budesonide treatment group 36 days after OVA challenge （ 7 days after budesonide discontinuance） . TSLP expression in the lung tissues was significantly lower in the budesonide treatment group than that in the asthma control group both 29 and 36 days after OVA challenge （ P 0. 05） . Conclusions Inhaled budesonide can inhibit the TSLP expression in the lung tissues and alleviate lung inflammatory reactions in asthmatic rats,but there is end-of-dose failure.