文献类型：期刊文献

中文题名：当归对阴虚哮喘小鼠气道黏液高分泌及TNF-α/NF-κB信号通路的影响

英文题名：Effects of Radix Angelicae Sinensis on airway mucus hypersecretion and the TNF-α/NF-κB signaling pathway in Yin-deficiency asthmatic mice

作者：姚楠[1];韦凌霞[1];王志旺[1,2];丁茂鹏[1];付晓艳[1];庞亚蓉[1];程小丽[1];蔺兴遥[1,2];邵晶[1]

第一作者：姚楠

机构：[1]甘肃中医药大学,兰州730000;[2]甘肃省中药药理与毒理学重点实验室,兰州730000

第一机构：甘肃中医药大学

年份：2020

期号：2

起止页码：97

中文期刊名：中国应用生理学杂志

外文期刊名：Chinese Journal of Applied Physiology

收录：CSTPCD;;Scopus;北大核心:【北大核心2017】；CSCD:【CSCD2019_2020】；PubMed;

基金：国家自然科学基金(81460668,81660653);甘肃省自然科学基金(1606RJZA011,1310RJZA086);甘肃省中药药理与毒理学重点实验室项目基金(ZDSYS-KJ-2018-001)

语种：中文

中文关键词：当归;阴虚哮喘;小鼠;黏液高分泌;α-肿瘤坏死因子(TNF-α);NF-κB

外文关键词：Radix Angelicae Sinensis(RADA);Yin-deficiency asthma;mouse;mucus hypersecretion;Alpha-tumor necrosis factor(TNF-α);NF-κB

摘要：目的:探讨当归对阴虚哮喘小鼠气道黏液高分泌及TNF-α/NF-κB信号通路的影响。方法:取KM小鼠随机分为空白对照组、模型对照组、氨溴索组、当归低、中、高剂量(2、4、8 g/kg)组(n=12),采用卵蛋白与甲状腺片复制阴虚哮喘模型,观测当归对小鼠哮喘症状、IgE、TNF-α以及肺组织Muc5ac与NF-κB表达的影响。结果:2、4、8 g/kg当归能明显缓解阴虚哮喘小鼠的哮喘症状,降低血清IgE与BALF中TNF-α水平,抑制肺组织Muc5ac与NF-κB的过度表达。结论:当归具有明显的平喘作用,抑制TNF-α/NF-κB信号通路而缓解气道黏液高分泌是其平喘的作用机制之一。
Objective:To investigate the therapeutic effects of Radix Angelicae Sinensis(RADA)on airway mucus hypersecretion and the tumor necrosis factor-α/nuclear factor-κB(TNF-α/NF-κB)signaling pathway in Yin-deficiency asthma mice.Methods:KM mice were randomly divided into control group,model group,ambroxol group and RADA low,medium and high dose(2,4 and 8 g/kg)group(n=12).Ovalbumin and the thyroid gland were used to replicate the model of Yin-deficiency asthma.Asthma symptoms in mice,immune globulin E(IgE),TNF-α,and the expressions of Mucin 5ac(Muc5ac)and NF-κB in lung tissue were observed under the intervention of RADA.Results:RADA at the doses of 2,4 and 8 g/kg could alleviate the asthma symptoms of Yin-deficiency asthma mice significantly,reduce the levels of IgE in serum and TNF-αin bronchoalveolar lavage fluid(BALF),and inhibite the overexpressions of Muc5ac and NF-κB in lung tissue.Conclusion:RADA has significant anti-asthmatic effect.One of its mechanisms is to inhibit TNF-α/NF-κB signaling pathway and to alleviate airway mucus hypersecretion.