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作 者:杨晋[1,2] 周瑶[1] 秦厚兵[1] 刘峰[1] 赵德育[1]
机构地区:[1]南京医科大学附属南京儿童医院呼吸病科,江苏省210008 [2]淮安市妇幼保健院儿科
出 处:《江苏医药》2013年第20期2392-2394,共3页Jiangsu Medical Journal
基 金:南京市医学科技发展项目(201108012)
摘 要:目的探讨支气管哮喘大鼠模型中磷酸酯酶与张力蛋白同源物(PTEN)-磷脂酰肌醇-3激酶(PI3K)通路的变化及布地奈德对其的影响。方法 40只SD大鼠随机均分为四组:正常对照(A)组、支气管哮喘模型(B)组、支气管哮喘加布地奈德干预(C)组和布地奈德(D)组。B、C组用卵清蛋白致敏和激发制成支气管哮喘大鼠模型,C、D组应用布地奈德雾化吸入。各组大鼠末次激发后24h内处死,计数支气管肺泡灌洗液(BALF)中细胞总数和嗜酸性粒细胞数,ELISA法测定BALF上清液中IL-13和TNF-α水平,RT-PCR检测各组大鼠肺组织中PTEN、AKT1的mRNA表达量。结果与A组相比,B组BALF中白细胞总数、嗜酸性粒细胞数、IL-13和TNF-α水平升高(P<0.05),肺组织中PTEN mRNA表达量降低,AKT1mRNA表达量升高(P<0.05)。与B组相比,C组BALF中白细胞总数、嗜酸性粒细胞数、IL-13和TNF-α水平降低(P<0.05),肺组织中PTEN表达量升高,AKT1表达量降低(P<0.05)。结论 PTEN-PI3K通路可能在支气管哮喘的发病及干预中起重要作用。Objective To investigate the changes of phosphatase and tensin homologue (PTEN)-phosphoinositide 3-kinase (PI3K) pathway in the routine model with bronchial asthma. Methods Forty SD rats were equally randomized into four groups of A(normal controls) ,B(bronchial asthma model made by ovalbumin sensitization and challenge), C (bronchial asthma model plus budesonide inhalation) and D(budesonide inhalation). All rats were killed within 24 hours after the last challenge. The total number of cells and the number of eosinophils in bronchoalveolar lavage fluid (BALF) of the left lung were counted. The levels of IL-13 and TNF-alpha in BALF supernatant were determined by ELISA. The expressions of PTEN and AKT1 mRNA in lung tissues were detected by RT-PCR. Results Compared with group A, the total number of cellS, the number of eosinophils and the levels of IL-13 and TNF-alpha were increased in BALF(P〈0. 05), and the expression of PTEN mRNA was decreased, while the expression of AKT1 mRNA was increased in lung tissues in group B (P〈0. 05). Compared with group B, the total number of cells, the number of eosinophils and the levels of IL-13 and TNF-alpha were decreased in BALF(P〈0.05) ,and the expression of PTEN mRNA was increased, while the expression of AKT1 mRNA was decreased in lung tissues in group C(P〈0. 05). Conclusion PTEN-PI3K pathway may play an important role in the pathogenesis and interventions of bronchial asthma.
关 键 词:支气管哮喘 磷酸酯酶与张力蛋白同源物 布地奈德
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