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粒细胞—巨噬细胞集落刺激因子对人气道平滑肌细胞内皮素…
引用本文:徐军 任筱兰. 粒细胞—巨噬细胞集落刺激因子对人气道平滑肌细胞内皮素…[J]. 中华结核和呼吸杂志, 1997, 20(5): 276-279
作者姓名:徐军 任筱兰
摘    要:目的 观察炎前细胞因子粒细胞-巨噬细胞集落刺激因子(GM-CSF)对培养的人气道平滑肌细胞内皮素-1(ET-1)基因及内皮素转换酶(ECE)基因表达的影响及茶碱对此种表达的作用,探讨在炎症环境下气道平滑肌细胞在气道高反应性发生,发展中的作用及低剂量茶碱在遏制气道高反应性的可能机制。方法 分别以GM-CSF(1000μg/ml)或与茶碱(125ng/ml)联合刺激离体培养人气道平滑肌细胞8小时,运用

关 键 词:平滑肌细胞 内皮素1 GM-CSF 基因表达 茶碱 哮喘

The effect of GM-CSF on endothelin-1 and endothelin converting enzyme gene expression in human airway smooth muscle cells with or without theophylline incubation]
J Xu,X Ren,N Zhong. The effect of GM-CSF on endothelin-1 and endothelin converting enzyme gene expression in human airway smooth muscle cells with or without theophylline incubation][J]. Chinese journal of tuberculosis and respiratory diseases, 1997, 20(5): 276-279
Authors:J Xu  X Ren  N Zhong
Affiliation:Guangzhou Institute of Respiratory Disease.
Abstract:OBJECTIVE: To explore the role of airway smooth muscle cells (ASMC) stimulated by inflammatory factors in the development of asthma and bronchial hyperresponsiveness (BHR) and the possible mechanism of low dose theophylline in the treatment of airway inflammation, the effects of GM-CSF on endothelin-1 and endothelin converting enzyme (ECE) gene expression in human ASMC and theophylline on their expressions were investigated. METHOD: The cultured human ASMCs were treated with GM-CSF (1,000 micrograms/ml), GM-CSF plus theophylline (125 ng/ml) respectively for 8 hours. Endothelin-1 and ECE gene expresion were measured by RT-PCR. RESULT: There was no ET-1 gene expression in control group, but strong expression in GM-CSF treated group; theophylline entirely inhibited GM-CSF induced ET-1 gene expression in the ASMC; no significant difference of ECE gene expression was found in three groups. CONCLUSION: GM-CSF causes a strong ET-1 gene expression but not ECE gene expression in cultured human airway smooth muscle cells; theophyllin inhibites this abnormal expression which may be one of the anti-inflammatory mechanisms of low dose theophylline in the management of chronic airway inflammation.
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