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雷公藤甲素对哮喘小鼠气道重塑及对STAT6、eotaxin的影响

张炜 黄林洁 陈茗

实用医学杂志2016,Vol.32Issue(20):3360-3363,4.
实用医学杂志2016,Vol.32Issue(20):3360-3363,4.DOI:10.3969/j.issn.1006-5725.2016.20.022

雷公藤甲素对哮喘小鼠气道重塑及对STAT6、eotaxin的影响

Effects of triptolide on airway remodeling as well as on STAT6 and eotaxin in asthmatic mice

张炜 1黄林洁 2陈茗2

作者信息

  • 1. 518055 深圳市南山区西丽人民医院呼吸内科
  • 2. 510120 广州市,中山大学孙逸仙纪念医院呼吸内科
  • 折叠

摘要

Abstract

Objective To investigate the effect of triptolide on asthmatic airway remodeling and signal transducer and activator of transcription 6 (STAT6), acid neutrophil chemokines (eotaxin) impact. Methods The total of 30 mice with ovalbumin (OVA) model of asthma were randomly divided into three groups, control group, asthma group and triptolide group. After 24 hours of the last shot, lung tissue was stained Bronchial inflammatory cell infiltration was determined by using semi-quantitative method and calculate the proportion of goblet cells in airway epithelial cells. Hydroxyproline was determined by McMillan airway mucus score. The mRNA level and protein level of STAT6 and eotaxin in airway epithelium were determined by RT-PCR and immunohistochemistry. Results Compared with asthma group, peribronchial inflammatory cells infiltration of triptolide group were reduced, which mucus index is (1.31 ± 0.23) and hydroxyproline is (284 ± 13) μmg/100 mg. it had a significant in asthma group (P < 0.05). Besides, the protein level and mRNA level of STAT6 and eotaxin were significantly decreased (P < 0.05). Moreover, it was a positive correlation between STAT6 and eotaxin level in airway epithelial (r = 0.668, P < 0.05). Conclusion Triptolide can inhibit airway remodeling and might through the down regulation of STAT6 and eotaxin expression.

关键词

雷公藤甲素/哮喘/气道重塑/STAT6/Eotaxin

Key words

Triptolide/Asthma/Airway remodeling/STAT6/Eotaxin

引用本文复制引用

张炜,黄林洁,陈茗..雷公藤甲素对哮喘小鼠气道重塑及对STAT6、eotaxin的影响[J].实用医学杂志,2016,32(20):3360-3363,4.

基金项目

广东省自然科学基金 ()

实用医学杂志

OA北大核心CSTPCD

1006-5725

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