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机构地区:[1]中国医科大学附属盛京医院小儿呼吸内科,沈阳110004
出 处:《中国小儿急救医学》2009年第6期558-560,共3页Chinese Pediatric Emergency Medicine
基 金:基金项月:辽宁省教育厅科学研究项目(20060953)
摘 要:目的探讨普米克令舒对哮喘大鼠气道平滑肌细胞NK1受体表达的影响。方法将45只Wistar大鼠随机分成正常对照组、哮喘组、普米克令舒治疗组,每组15只。用雾化吸入卵蛋白制作哮喘大鼠模型,治疗组吸入卵蛋白诱发哮喘后给予普米克令舒吸入治疗。第21天取大鼠气道平滑肌细胞原代培养。用体外培养纯化的第4代细胞定量PCR检测各组气道平滑肌细胞NK-1受体mRNA表达差异。结果普米克令舒治疗组气道平滑肌细胞NK-1受体mRNA相对含量为1.0820±0.1146,较哮喘组(1.1687±0.1356)明显降低.但高于正常对照组(1.0347±0.2503),差异均有显著性(P〈0.05)。结论NK-1受体通过增加哮喘的神经源性炎症参与哮喘的发病机制。普米克令舒抑制哮喘大鼠气道神经源性炎症的作用与降低NK-1受体表达有关。Objective To investigate the effect of budesonide on NK-1 receptor expression in airway smooth muscle cell (ASMC). Methods According to the random method,45 wistar rats were divided into three groups:asthmatic group,budesonide treatment group and control group. Aerosolize ovalbumin was used to make asthmatic rat model. Budesonide treatment group were given budesonide after inhaled ovalbumin. On day 21 ,primary rat ASMC culture was conducted. The fourth cell passage and purified ASMC was collected for RT-PCR. The content of NK-1R was determined by real-time quantitative PCR. Data were expressed as mean ± standard error ( SE). The ANOVE Tukey test was carried out by using SPSS17.0 software and P 〈 0. 05 was considered significant. Results As compared with that of asthmatic group ( 1. 168 7 ± 0. 135 6 ), NK-1R mRNA in therapy group ( 1. 082 0 ± 0. 114 6 ) decreased significantly ( P 〈 0. 05 ) , but remained still higher than that of control group( 1. 034 7 ± 0. 250 3 ) ( P 〈 0. 05 ). Conclusion NK-1R may be involved in the pathogenesis of asthma. Budesonide may down-regulate the expression of the NK-1R mRNA in the airway smooth muscle cell, which may inhibit inflammation in asthmatic attacks.
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