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虾原肌球蛋白联合脂多糖诱导的小鼠哮喘气道炎症模型的研究

高翔 莫艳 朱嘉豪 董耀 陈永鑫 徐良玉 侯瑞涛 方蕾

扬州大学学报(农业与生命科学版)2024,Vol.45Issue(3):55-63,9.
扬州大学学报(农业与生命科学版)2024,Vol.45Issue(3):55-63,9.DOI:10.16872/j.cnki.1671-4652.2024.03.006

虾原肌球蛋白联合脂多糖诱导的小鼠哮喘气道炎症模型的研究

A model of airway inflammation in asthma mice induced by shrimp tropomyosin plus lipopolysaccharide

高翔 1莫艳 2朱嘉豪 1董耀 1陈永鑫 1徐良玉 1侯瑞涛 1方蕾1

作者信息

  • 1. 扬州大学医学院,江苏扬州 225009
  • 2. 广西壮族自治区妇幼保健医院广西儿科疾病临床医学研究中心,南宁 530000
  • 折叠

摘要

Abstract

Aim to definite the type of asthma model induced by lipopolysaccharide(LPS)combined with allergens.We established a mouse model of asthmatic airway inflammation induced by shrimp tropomyosin(ST)plus LPS and compared this model with models induced by ovalbumin(OVA)plus complete Freund's adjuvant(CFA)for neutrophilic asthma or ST combined with aluminum adjuvant for eosinophilic asthma.Compared to the control group,ST plus LPS induced the increased airway inflammation,airway epithelial mucus secretion,and total cell count in BALF.Lung IL-17A protein lev-el and IL-1β,IL-5,IL-17A,Eotaxin,and Mu5ac mRNA expression in lung tissue were elevated,while the protein ex-pression of E-CDH in airway epithelium and the mRNA expression of Cdh1 in the lung tissues were decreased.The pro-tein expression of ARG-1 around the airway and the mRNA level of Arg-1 in the lung tissues were increased.DEX treat-ment partially improved airway inflammation,excessive mucus secretion,and cytokine levels induced by ST combined with LPS,but DEX had no significant effect on the expression of Cdhl,IL-5,and IL-1β in lung tissue.In conclusion,the model in-duced by ST plus LPS might be an animal model of the advanced stage from eosinophil asthma to neutrophilic asthma.

关键词

哮喘/气道炎症/虾原肌球蛋白/脂多糖/卵清蛋白

Key words

asthma/airway inflammation/shrimp tropomyosin/lipopolysaccharide/ovalbumin

分类

农业科技

引用本文复制引用

高翔,莫艳,朱嘉豪,董耀,陈永鑫,徐良玉,侯瑞涛,方蕾..虾原肌球蛋白联合脂多糖诱导的小鼠哮喘气道炎症模型的研究[J].扬州大学学报(农业与生命科学版),2024,45(3):55-63,9.

基金项目

江苏省卫健委科研基金面上项目(M2022034) (M2022034)

扬州大学大学生科创项目(XCX20230830) (XCX20230830)

扬州大学学报(农业与生命科学版)

OA北大核心CSTPCD

1671-4652

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