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当归对阴虚哮喘小鼠模型Th17优势免疫应答的影响     被引量:7

Effects of Radix Angelicae Sinensis on Th17 dominant immune response in asthmatic mice with Yin deficiency syndrome

文献类型:期刊文献

中文题名:当归对阴虚哮喘小鼠模型Th17优势免疫应答的影响

英文题名:Effects of Radix Angelicae Sinensis on Th17 dominant immune response in asthmatic mice with Yin deficiency syndrome

作者:王志旺[1,2];妥海燕[1];任远[1,2];程小丽[3];刘雪枫[1];李荣科[4]

第一作者:王志旺

机构:[1]甘肃中医药大学药学院,兰州730000;[2]甘肃省中药药理与毒理学重点实验室,兰州730000;[3]甘肃中医药大学教学实验中心,兰州730000;[4]甘肃中医药大学基础医学院,兰州730000

第一机构:甘肃中医药大学药学院(西北中藏药协同创新中心办公室)

年份:2016

卷号:32

期号:1

起止页码:38

中文期刊名:免疫学杂志

外文期刊名:Immunological Journal

收录:CSTPCD;;北大核心:【北大核心2014】;CSCD:【CSCD2015_2016】;

基金:国家自然科学基金(81460668);甘肃省自然科学基金(1310RJZA086)

语种:中文

中文关键词:当归;阴虚哮喘;Balb/c小鼠;Th17优势免疫应答

外文关键词:Radix Angelicae Sinensis; Asthma with Yin deficiency syndrome; Balb/c mouse; Th17 dominant immune response

摘要:目的探讨当归对阴虚哮喘Balb/c小鼠模型Th17细胞优势免疫应答的影响。方法通过注射OVA致敏后吸入OVA激发的方法来复制Balb/c小鼠哮喘模型,实验后期灌胃甲状腺素复制阴虚哮喘模型,通过观测小鼠哮喘行为学、血清及BALF中IL-17A、TNF-α的水平、肺组织及BALF中炎性细胞的含量、肺组织中RORγt蛋白表达水平,探讨当归的平喘作用及对Th17细胞优势免疫应答的影响。结果 2~8 g/kg当归可明显减少阴虚哮喘小鼠哮喘发作的鼠数及其发作症状,缓解肺组织病理学变化而减少肺组织及BALF中炎性细胞的数量,降低血清及BALF中IL-17A及TNF-α的水平,抑制肺组织中RORγt蛋白的表达(P〈0.05,0.01);同时,当归与地塞米松配伍后对嗜酸粒细胞、IL-17A及RORγt的抑制作用具有一定的协同作用(P〈0.05,0.01)。结论当归具有一定的平喘作用,抑制IL-17、TNF-α与RORγt而缓解Th17优势免疫应答是其作用机制之一。
To investigate therapeutic effects of Radix Angelicae Sinensis(RASI) in asthmatic disease with Yindeficiency syndrome, a Balb/c mouse model of asthma was established with ovalbumin. Thyroxin was administeredthereafter to create the disease model of Yin deficiency syndrome. The results showed that 2-8 g/kg RASI could easeasthmatic symptoms and reduce number of inflammatory cells in BALF and lung tissue of model mice. Themechanism of the therapeutic effects may related to the inhibiting effects of RASI on Th17 cell accumulation andresponse in lung tissue(P〈0.05, 0.01). In addition, RASI and DXM have synergistic effect in inhibitingeosinophilic cell recruitment. In conclusion, RASI has some anti-asthma effect and one of the mechanisms isinhibiting Th17 dominant immune response through depressing IL-17, TNF-α and RORγt.

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