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吸入性皮质类固醇抑制哮喘大鼠气道平滑肌细胞中 P 物质受体的表达。

Inhaled corticosteroids inhibit substance P receptor expression in asthmatic rat airway smooth muscle cells.

机构信息

Department of pediatrics, Shengjing hospital of China Medical University, Shenyang 110004, China.

出版信息

BMC Pulm Med. 2012 Dec 17;12:79. doi: 10.1186/1471-2466-12-79.

Abstract

BACKGROUND

Neurokinins (NKs) participate in asthmatic airway inflammation, but the effects of NKs on airway smooth muscle cells (ASMCs) and those of corticosteroids on NKs are unknown.

METHODS

To investigate the effect of budesonide on substance P (NK-1) receptor (NK-1R) expression in the lung and ASMCs, 45 Wistar rats were randomly divided into three groups: control, asthmatic, and budesonide treatment. Aerosolized ovalbumin was used to generate the asthmatic rat model, and budesonide was administered after ovalbumin inhalation. On day 21, bronchial responsiveness tests, bronchoalveolar lavage, and cell counting were conducted. NK-1R protein expression in the lung was investigated by immunohistochemistry and image analysis. Primary rat ASMC cultures were established, and purified ASMCs of the fourth passage were collected for mRNA and protein studies via real-time RT-PCR, immunocytochemistry, and image analysis.

RESULTS

NK-1R mRNA and protein expression in the budesonide treatment group rat's lung and ASMCs were less than that in the asthmatic group but greater than that in the control group.

CONCLUSIONS

NK-1R is involved in the pathogenesis of asthma and that budesonide may downregulate the expression of NK-1R in the ASMCs and airways of asthmatic rats, which may alleviate neurogenic airway inflammation.

摘要

背景

神经激肽(NKs)参与哮喘气道炎症,但 NKs 对气道平滑肌细胞(ASMCs)的影响以及皮质类固醇对 NKs 的影响尚不清楚。

方法

为了研究布地奈德对肺部和 ASMCs 中 P 物质(NK-1)受体(NK-1R)表达的影响,将 45 只 Wistar 大鼠随机分为三组:对照组、哮喘组和布地奈德治疗组。雾化卵白蛋白用于生成哮喘大鼠模型,在卵白蛋白吸入后给予布地奈德。第 21 天,进行支气管反应性测试、支气管肺泡灌洗和细胞计数。通过免疫组织化学和图像分析研究肺部 NK-1R 蛋白表达。建立原代大鼠 ASMC 培养物,并收集第 4 代纯化的 ASMC 进行实时 RT-PCR、免疫细胞化学和图像分析的 mRNA 和蛋白质研究。

结果

布地奈德治疗组大鼠肺和 ASMCs 中的 NK-1R mRNA 和蛋白表达均低于哮喘组,但高于对照组。

结论

NK-1R 参与哮喘的发病机制,布地奈德可能下调哮喘大鼠 ASMCs 和气道中 NK-1R 的表达,从而减轻神经源性气道炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49a7/3579708/e04bb93e132d/1471-2466-12-79-1.jpg

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