程静,年瑞,李万军.miR-33a基于Notch信号通路对幼年哮喘小鼠Th17/Treg细胞平衡的影响.[J].中南医学科学杂志.,2023,(2):202-205, 225.
miR-33a基于Notch信号通路对幼年哮喘小鼠Th17/Treg细胞平衡的影响
Effect of miR-33a on Th17/Treg cell balance in juvenile asthma mice based on Notch signal pathway
投稿时间:2022-05-25  修订日期:2023-02-21
DOI:10.15972/j.cnki.43-1509/r.2023.02.011
中文关键词:  miR-33a  哮喘  Th17/Treg  Notch信号通路 [
英文关键词:miR-33a  asthma  Th17/Treg  Notch pathway
基金项目:2022年3201医院科研基金项目(3201yk202247)
作者单位E-mail
程静 西安交通大学医学院附属3201医院病理科,陕西汉中723000 e-mail为chengj199101@126.com,e-mail为lwjdf163@163.com 
年瑞 西安交通大学医学院附属3201医院病理科,陕西汉中723000  
李万军 西安交通大学医学院附属3201医院病理科,陕西汉中723000 e-mail为chengj199101@126.com,e-mail为lwjdf163@163.com 
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中文摘要:
      目的探究miR-33a通过调控Notch信号通路对幼年哮喘小鼠辅助性T细胞17(Th17)/调节性T细胞(Treg)平衡的影响。 方法小鼠随机分为对照组、哮喘组和miR-33a组(哮喘+miR-33a)。qRT-PCR检测各组肺组织miR-33a水平。比较各组大鼠气道阻力、Th17/Treg细胞平衡及其细胞因子、淋巴细胞Notch信号通路的水平。 结果与对照组比较,哮喘组肺组织miR-33a降低,气道阻力和肺组织损伤程度升高,Th17、Th17/Treg、白细胞介素-17及Notch信号通路水平升高,Treg水平降低(P<0.05);而与哮喘组比较,miR-33a组上述趋势均得到逆转(P<0.05)。 结论miR-33a可通过抑制Notch信号通路,使Th17/Treg平衡向Treg偏移,从而改善哮喘小鼠气道反应性。
英文摘要:
      AimTo explore the effect of miR-33a on the balance of helper T cell 17 (Th17)/regulatory T cell (Treg) in juvenile asthma mice by regulating the Notch pathway. MethodsThe mice were randomly divided into control group, asthma group and miR-33a group (asthma+miR-33a). The level of miR-33a in lung tissue of each group was detected by qRT-PCR. Compare the levels of airway resistance, the levels of airway resistance, Th17/Treg cell balance, cytokines and Notch pathway in lymphocytes were compared in each group. ResultsCompared with the control group, the lung tissue miR-33a in the asthma group decreased, the airway resistance and the degree of lung tissue injury increased, the levels of Th17, Th17/Treg, interleukin-17 and Notch pathway increased, and the level of Treg decreased (P<0.05). Compared with the asthma group, the above trends in the miR-33a group were reversed (P<0.05). ConclusionmiR-33a can shift Th17/Treg balance to Treg by inhibiting Notch pathway, thus improving airway responsiveness of asthma mice.
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