哮喘患者肺组织中速激肽受体基因表达增加及其受类固醇的调节。
Increased tachykinin receptor gene expression in asthmatic lung and its modulation by steroids.
作者信息
Adcock I M, Peters M, Gelder C, Shirasaki H, Brown C R, Barnes P J
机构信息
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
出版信息
J Mol Endocrinol. 1993 Aug;11(1):1-7. doi: 10.1677/jme.0.0110001.
Substance P has several inflammatory effects on the airways mediated via neurokinin 1 receptors (NK1Rs) and, if released from sensory nerves, may amplify the chronic inflammation seen in asthma. Northern blot analysis of NK1R mRNA in lung showed a 52 +/- 10% (S.E.M.; P < 0.01) increase in mRNA in the asthmatic lung compared with non-asthmatic control tissue. NK1R mRNA was reduced by 84.5 +/- 1.9% after incubation with dexamethasone (1 microM) for 3 h (P < 0.01). In contrast, NK2R mRNA was unaltered in asthmatic lungs and dexamethasone treatment had no effect on the level of NK2R mRNA. These results suggest that chronic inflammation in asthma may result in increased NK1R gene expression and that this effect is reversed by glucocorticosteroids.
P物质对气道具有多种经由神经激肽1受体（NK1Rs）介导的炎症作用，并且如果从感觉神经释放，可能会放大哮喘中所见的慢性炎症。对肺中NK1R mRNA的Northern印迹分析显示，与非哮喘对照组织相比，哮喘肺中的mRNA增加了52±10%（标准误；P<0.01）。与地塞米松（1μM）孵育3小时后，NK1R mRNA降低了84.5±1.9%（P<0.01）。相比之下，哮喘肺中的NK2R mRNA未改变，地塞米松处理对NK2R mRNA水平没有影响。这些结果表明，哮喘中的慢性炎症可能导致NK1R基因表达增加，并且这种作用可被糖皮质激素逆转。
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