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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 phosphatidylinositol and tensin homolog (PTEN) - phosphatidylinositol 3 - kinase (PI3K) pathway in bronchial asthma rat model and the effect of budesonide on it. Methods Forty SD rats were randomly divided into four groups: normal control group (A), bronchial asthma model group (B), bronchial asthma with budesonide intervention group (C) and budesonide group (D). B, C group with ovalbumin sensitization and excitation of bronchial asthma rat model, C, D group budesonide inhalation. The rats in each group were sacrificed within 24h after the last challenge. The total number of cells and eosinophils in bronchoalveolar lavage fluid (BALF) were counted. The levels of IL-13 and TNF-α in BALF supernatants were determined by ELISA. RT- The mRNA expression of PTEN and AKT1 in the lung tissue of each group was detected. Results Compared with group A, the total number of leukocytes, eosinophils, IL-13 and TNF-α in BALF of group B were increased (P <0.05), the expression of PTEN mRNA and the expression of AKT1 mRNA in lung tissue were increased (P <0.05). Compared with group B, the total number of leukocytes, eosinophils, levels of IL-13 and TNF-α in BALF in group C were decreased (P <0.05), and the expression of PTEN in lung tissue was increased and the expression of AKT1 was decreased in group C (P < 0.05). Conclusion PTEN-PI3K pathway may play an important role in the pathogenesis and intervention of bronchial asthma.