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雷帕霉素对哮喘小鼠气道重塑的影响

延光海 金光玉 朴红梅 郑明昱 李良昌 李光昭

中国药理学通报2013,Vol.29Issue(7):942-946,5.
中国药理学通报2013,Vol.29Issue(7):942-946,5.DOI:10.3969/j.issn.1001-1978.2013.07.013

雷帕霉素对哮喘小鼠气道重塑的影响

Effects of rapamycin on airway remodeling in asthmatic mice

延光海 1金光玉 2朴红梅 2郑明昱 3李良昌 1李光昭1

作者信息

  • 1. 延边大学医学院解剖学教研部,吉林,延吉,133002
  • 2. 延边大学附属医院呼吸内科,吉林,延吉,133002
  • 3. 延边大学中医学院内科学教研室,吉林,延吉,133002
  • 折叠

摘要

Abstract

Aim To explore the effect of rapamycin on airway remodeling and the expression of mTOR in asthmatic mice. Methods Thirty male BABL/c mice were randomly divided into three groups with 10 mice in each group : control group , OVA group , and rapamycin group. The left lung was isolated for pathological examination. Lung sections were stained with HE and PAS ,immunohistochemistry. The concentrations of IL-4,IL-5,IL-3 in BALF were examined by ELISA, and the mTOR from the right lung tissues was detected by Western blot. The changes of the airway resistance and lung function were analyzed by means of animal lungs function analysis system. Results In OVA group, the number of inflammatory cells and the concentrations of IL-4, IL-5 , IL-3 in BALF and bronchial airway thickness , bronchial smooth muscle thickness, and mTOR in lung tissue were significantly higher than those in control group ( P < 0. 05 ). In rapamycin group, the number of inflammatory cells, the concentrations of IL-4 , IL-5 , IL-3 in BALF and bronchial airway thickness , bronchial smooth muscle thickness, and mTOR in lung tissue were significantly lower than those in OVA group ( P < 0. 05 ). The above indices of Rapamycin group were significantly lower than those of OVA group ( P < 0. 05 ). Conclusion Rapamycin can inhibit the development of airway remodeling in asthmatic mice, and the possible mechanism may be due to its inhibition of mTOR signaling.

关键词

支气管哮喘/气道重塑/雷帕霉素/mTOR/IL-4/IL-5/IL-13

Key words

asthma/ airway remodeling/ rapamycin/ mTOR/ IL-4/IL-5/IL-3

分类

医药卫生

引用本文复制引用

延光海,金光玉,朴红梅,郑明昱,李良昌,李光昭..雷帕霉素对哮喘小鼠气道重塑的影响[J].中国药理学通报,2013,29(7):942-946,5.

基金项目

国家自然科学基金资助项目(No 81060003,81260665) (No 81060003,81260665)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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