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Zhongguo Dang Dai Er Ke Za Zhi ; 18(7): 614-7, 2016 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-27412544

RESUMO

OBJECTIVE: To study the expression profiles of PI3K, NF-κB, and STAT1 in peripheral blood mononuclear cells (PBMCs) in children with bronchial asthma, as well as their roles in the pathogenesis of asthma. METHODS: Thirty children with acute exacerbation of bronchial asthma were enrolled as the asthma group, and 20 healthy children were enrolled as the control group. RT-PCR and Western blot were used to measure the mRNA and protein expression levels of PI3K, NF-κB, and STAT1 in PBMCs. A spirometer was used to compare the pulmonary function between the two groups. The correlations between the mRNA expression of PI3K, NF-κB, and STAT1 and pulmonary function in children with bronchial asthma were analyzed. RESULTS: The asthma group had significantly higher mRNA and protein expression levels of PI3K, NF-κB, and STAT1 than the control group (P<0.05). Compared with the control group, the asthma group showed significant reductions in pulmonary function indices such as FEV1%, FEV1/FVC, and PEF% (P<0.05). In children with bronchial asthma, the mRNA expression levels of PI3K, NF-κB, and STAT1 were negatively correlated with FEV1%, FEV1/FVC, and PEF% (P<0.05). CONCLUSIONS: The expression levels of PI3K, NF-κB, and STAT1 increase in children with asthma, and are negatively correlated with pulmonary function indices, suggesting that PI3K, NF-κB and STAT1 are involved in the development and progression of bronchial asthma in children.


Assuntos
Asma/etiologia , Leucócitos Mononucleares/química , NF-kappa B/fisiologia , Fosfatidilinositol 3-Quinases/fisiologia , Fator de Transcrição STAT1/fisiologia , Asma/sangue , Asma/fisiopatologia , Criança , Pré-Escolar , Feminino , Volume Expiratório Forçado , Humanos , Masculino , NF-kappa B/sangue , NF-kappa B/genética , Fosfatidilinositol 3-Quinases/sangue , Fosfatidilinositol 3-Quinases/genética , RNA Mensageiro/análise , Fator de Transcrição STAT1/sangue , Fator de Transcrição STAT1/genética
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