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苦味素受体对大气可吸入颗粒诱导的气道黏液高分泌干预机制研究

刘峰 周向东 李琪 刘美花 王杰

中国药业2018,Vol.27Issue(21):5-8,4.
中国药业2018,Vol.27Issue(21):5-8,4.DOI:10.3969/j.issn.1006-4931.2018.21.002

苦味素受体对大气可吸入颗粒诱导的气道黏液高分泌干预机制研究

Study on Intervention Mechanism of Bitter Taste Receptors on Airway Mucous Hypersecretion Induced by Atmospheric Inhalable Particles

刘峰 1周向东 1李琪 1刘美花 1王杰1

作者信息

  • 1. 海南医学院第一附属医院呼吸内科, 海南 海口 570102
  • 折叠

摘要

Abstract

Objective To investigate the mechanism of bitter taste receptor (T2 Rs) on mucin hypersecretion induced by particles with an aerodynamic diameters of less than 2. 5 μm (PM2. 5) in airway epithelial cells. Methods Bronchial epithelial cells were cultured to construct the model of airway mucus hypersecretion, and then stimulated by PM2. 5, platycodin was taken as intervention factor. The expressions of T2 R14 and MUC5 AC protein were detected by immunofluorescence method and ELISA method respectively. The levels of T2 R14 and MUC5 AC m RNA were measured by RT-PCR. Results The expression of MUC5 AC protein and level of MUC5 AC m RNA in the PM2. 5 group were significantly higher than those in the control group, the expression of T2 R14 protein and level of T2 R14 m RNA were not changed obviously. The expression of MUC5 AC protein and level of MUC5 AC m RNA in platycodin intervention group were significantly lower than those in PM2. 5 group, while the expression of T2 R14 protein and level of T2 R14 m RNA were significantly higher than those in the control group. Conclusion The components of bitter Chinese medicine may induce activating and expressing of human bronchial epithelial cells T2 R14, and then inhibit the airway hypersecretion via blocking MUC5 AC production and secretion.

关键词

苦味素受体/PM2.5/黏蛋白5AC/气道黏液高分泌

Key words

bitter taste receptor/PM2.5/MUC5AC/airway mucous hypersecretion

分类

医药卫生

引用本文复制引用

刘峰,周向东,李琪,刘美花,王杰..苦味素受体对大气可吸入颗粒诱导的气道黏液高分泌干预机制研究[J].中国药业,2018,27(21):5-8,4.

基金项目

国家自然科学基金[81660010] ()

国家自然科学基金[8161101480] ()

海南省自然科学基金[20168305] ()

海南省卫生厅科研课题[16A200021] ()

海南医学院培育基金[HY2016-16] ()

中国药业

OACSTPCD

1006-4931

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