论文部分内容阅读
目的:探讨磷脂酰肌醇3激酶(PI3K)抑制剂wortmannin对哮喘大鼠支气管上皮细胞诱导型一氧化氮合酶(iNOS)表达的影响。方法:24只成年哮喘大鼠随机分成对照组、哮喘组以及PI3K抑制剂wortmannin干预组。对支气管肺泡灌洗液(BALF)细胞总数及嗜酸性粒细胞进行计数,免疫组织化学检测大鼠支气管上皮细胞iNOS蛋白的表达,RT-PCR检测肺组织iNOSmRNA的表达,分光光度计检测肺组织PI3K活性、iNOS活性及NO含量。结果:哮喘组大鼠BALF细胞总数计数及嗜酸性粒细胞分类均高于对照组;PI3K抑制剂wortmannin干预组BALF嗜酸性粒细胞计数及分类明显低于哮喘组,差异显著。哮喘组肺组织PI3K活性、iNOS活性及NO含量高于对照组,PI3K抑制剂wortmannin干预组肺组织PI3K活性、iNOS活性及NO含量低于哮喘组。哮喘组大鼠支气管上皮细胞iNOS蛋白及肺组织iNOS mRNA表达较对照组明显增强,但PI3K抑制剂wortmannin组iNOS蛋白及mRNA表达均明显弱于哮喘组。结论:PI3K可调节哮喘大鼠气道iNOS表达,影响哮喘气道炎症反应。
AIM: To investigate the effect of phosphatidylinositol 3 - kinase (PI3K) inhibitor wortmannin on the expression of inducible nitric oxide synthase (iNOS) in bronchial epithelial cells of asthmatic rats. Methods: Twenty-four adult asthmatic rats were randomly divided into control group, asthma group and PI3K inhibitor wortmannin intervention group. The total number of bronchoalveolar lavage fluid (BALF) cells and eosinophils were counted. The expression of iNOS protein in bronchial epithelial cells was detected by immunohistochemistry. The expression of iNOS mRNA in lung tissue was detected by RT-PCR. The expression of PI3K Activity, iNOS activity and NO content. Results: The total count of BALF cells and the classification of eosinophils in asthmatic rats were higher than those in control group. The numbers and classification of BALF eosinophils in wortmannin-treated PI3K inhibitor group were significantly lower than those in asthma group. PI3K activity, iNOS activity and NO content in lung tissue of asthmatic group were higher than those in control group. PI3K activity, iNOS activity and NO content in lung tissue of PI3K inhibitor wortmannin intervention group were lower than those in asthma group. The expression of iNOS protein and iNOS mRNA in bronchial epithelial cells of bronchial epithelial cells of asthmatic rats were significantly increased compared with that of the control group. However, the expression of iNOS protein and mRNA of bronchial epithelial cells in asthmatic rats was significantly weaker than that in asthma rats. Conclusion: PI3K can regulate the expression of iNOS in airway of asthmatic rats and affect airway inflammation in asthmatic rats.