[1]王媛媛,王桂玲,耿雨作,等.黄芪多糖通过TGF-β1/Smads通路对哮喘大鼠Th1/Th2免疫失衡的调节作用[J].陕西中医,2024,(9):1181-1185.[doi:DOI:10.3969/j.issn.1000-7369.2024.09.006]
　WANG Yuanyuan,WANG Guiling,GENG Yuzuo,et al.Effects of Astragalus polysaccharide on Th1/Th2 immune imbalance in asthmatic rats through TGF-β1/Smads pathway[J].,2024,(9):1181-1185.[doi:DOI:10.3969/j.issn.1000-7369.2024.09.006]
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黄芪多糖通过TGF-β1/Smads通路对哮喘大鼠Th1/Th2免疫失衡的调节作用
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《陕西中医》[ISSN:1000-7369/CN:61-1281/TN]

卷:
期数:
2024年9期
页码:
1181-1185
栏目:
基础研究
出版日期:
2024-09-05

文章信息/Info

Title:
Effects of Astragalus polysaccharide on Th1/Th2 immune imbalance in asthmatic rats through TGF-β1/Smads pathway
作者:
王媛媛; 王桂玲; 耿雨作; 杨 江
(宿迁市中医院儿科,江苏 宿迁 223800)
Author(s):
WANG Yuanyuan; WANG Guiling; GENG Yuzuo; YANG Jiang
(Department of Pediatrics,Suqian Hospital of Traditional Chinese Medicine,Suqian 223800,China)
关键词:
黄芪多糖;  哮喘;  转化生长因子β1;  辅助性T细胞;  TGF-β1/Smads信号通路;  Th1/Th2
Keywords:
Astragalus polysaccharide;  Asthma;  Transforming growth factor β1;  T helper cells;  TGF-β1/Smads signaling pathway;  Th1/Th2
分类号:
R 256.12
DOI:
DOI:10.3969/j.issn.1000-7369.2024.09.006
文献标志码:
A
摘要:
目的:探讨黄芪多糖通过转化生长因子(TGF)-β1/Smads信号通路对哮喘大鼠辅助性T细胞(Th)l/Th2免疫失衡的调节作用。方法:选择雄性SD大鼠40只,分为对照组、模型组、黄芪多糖低、中、高剂量组,各8只。建立慢性哮喘大鼠模型,对照组和模型组大鼠尾静脉注射等体积0.9%氯化钠溶液,川芎嗪低、中、高剂量腹腔注射川芎嗪,各组均连续治疗14 d。干预后检测各组大鼠支气管黏膜受损面积和平滑肌厚度,收集各组大鼠支气管肺泡灌洗液(BALF),测定白细胞介素-4(IL-4)、干扰素-γ(IFN-γ)水平变化,苏木精-伊红(HE)染色观察肺组织结构变化,实时荧光定量PCR(qRT-PCR)和蛋白质免疫印迹(Western blot)对肺组织TGF-β1、Smad2、Smad3 mRNA和蛋白表达进行测定。结果:与对照组比较,模型组支气管黏膜受损面积、平滑肌厚度增加,与模型组比较,黄芪多糖各组均下降,且呈剂量依赖性(P<0.05)。与对照组比较,模型组BALF中IFN-γ水平降低,IL-4水平升高,与模型组比较,黄芪多糖各组BALF中IFN-γ水平均升高,IL-4水平均下降,且呈剂量依赖性(P<0.05)。模型组肺组织TGF-β1、Smad2、Smad3 mRNA和蛋白表达较对照组升高,黄芪多糖各组肺组织TGF-β1、Smad2、Smad3 mRNA和蛋白表达较模型组下降,且呈剂量依赖性(P<0.05)。结论:黄芪多糖通过抑制TGF-β1/Smads信号激活阻止哮喘大鼠气道炎症,调节Th1/Th2比值失衡,改善大鼠肺组织病理损伤。
Abstract:
Objective:To investigate the astragalus polysaccharides by transforming growth factor TGF(transforming growth factor)-β1/Smads signal pathway pathway to asthma rats helper T cells(T helper cell,Th)1 / Th2 immune imbalance adjustment.Methods:Forty male SD rats were selected and divided into control group,model group,Astragalus polysaccharide low-dose,medium-dose and high-dose groups(8 rats each group).The rat model of chronic asthma was established,and rats in the control group and model group were injected with equal volume of normal saline through tail vein,and tetramethylpyrazine was injected intraperitoneally at low,medium and high doses.All groups were treated continuously for 14 days.After intervention,the damaged bronchial mucosa area and smooth muscle thickness of rats in each group were detected,bronchoalveolar lavage fluid(BALF)was collected,and the changes of interleukin-4(IL-4)and interferon-γ(IFN-γ)levels were measured,and the changes of lung tissue structure were observed by hematoxylin-eosin(HE)staining.Real-time quantitative fluorescent PCR(qRT-PCR)and Western blot were used to determine the mRNA and protein expressions of TGF-β1,Smad2 and Smad3 in lung tissues.Results:Compared with the control group,the damaged area of bronchial mucosa and the thickness of smooth muscle in the model group were increased,and compared with the model group,the astragalus polysaccharide in each group were decreased,in a dose-dependent manner(P<0.05).Compared with the control group,IFN-γ level in BALF of the model group was decreased and IL-4 level was increased; compared with the model group,IFN-γ level in BALF of all Astragalus polysaccharide groups was increased and IL-4 level was decreased in a dose-dependent manner(P<0.05).The model group had significantly higher mRNA and protein expressions of TGF-β1,Smad2,and Smad3 in lung tissue than the control group,and the APS groups had significantly lower mRNA and protein expressions of TGF-β1,Smad2,and Smad3 than the model group in a dose-dependent manner(P<0.05).Conclusion:Astragalus polysaccharide can inhibit the activation of TGF-β1/Smads signal to prevent airway inflammation in asthmatic rats,regulate the imbalance of Th1/Th2 ratio,and improve the pathological injury of lung tissue in rats.

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备注/Memo

备注/Memo:
基金项目:江苏省中医药科技发展计划面上项目(MS2022132); 江苏省宿迁市自然科学基金资助项目(K202111)
更新日期/Last Update: 2024-09-09