Effect of phosphatidylinositol 3-kinase on inducible nitric oxide synthase in bronchiole epithelial cells of asthmatic rat
- VernacularTitle:磷脂酰肌醇3激酶对哮喘大鼠气道上皮细胞诱导型一氧化氮合酶表达的调控作用
- Author:
Xiaodong XIA
;
Hui XU
;
Liqin WU
;
Yuanrong DAI
;
Lei YANG
;
Zhengjie XU
- Publication Type:Journal Article
- Keywords:
Phosphatidylinositol 3-kinase;
Asthma;
Nitric oxide;
Nitric-oxide synthase;
Airway inflammation
- From:
Chinese Journal of Pathophysiology
2009;25(12):2381-2384
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effect of phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin on expression of inducible nitric oxide synthase (iNOS) in bronchiole epithelial cells of asthma rat.METHODS: 24 male Sprague-Dawley rats were randomly divided into 3 group, namely control group, asthma group and PI3K inhibitor wortmannin+asthma group. The numbers of total cells and eosinophil cells in bronchoalveolar lavage fluid (BALF) were counted. The expression of inducible nitric oxide synthase was detected by immunohistochemistry method, and iNOS mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). The activity of PI3K, iNOS and content of NO in lung homogenates were tested by spectrophotometry.RESULTS: The numbers of eosinophils and the ratios of eosinophils to total cells in BALF in asthma group were significantly higher than those in control group, while those in wortmannin+asthma group were decreased compared to asthma group. The activity of PI3K, iNOS and content of NO in lung homogenats in asthma group were significantly higher than those in control group, while those in wortmannin+asthma group were decreased compared to asthma group. The expression of iNOS protein in bronchiole epithelial cells and mRNA in lung homogenates in asthma group were markedly increased compared to control group, while those in wortmannin+asthma group were decreased compared to asthma group.CONCLUSION: PI3K regulates the expression of iNOS in airway of asthma rat and affects inflammatory reaction in airway.