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预防医学  2019, Vol. 31 Issue (10): 998-1001    DOI: 10.19485/j.cnki.issn2096-5087.2019.10.006
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黄芩苷体内抑制结核分枝杆菌的机制研究
赵丰权1, 戴建义1, 李君桦1, 蔡玉伟1, 董培红2
1.温州市中心医院感染科,浙江 温州 325000;
2.温州医科大学附属第一医院
Baicalin inhibit Mycobacterium tuberculosis in vivo by regulating the expression of Toll like receptor 4 and nuclear factor κB
ZHAO Feng-quan*, DAI Jian-yi, LI Jun-hua, CAI Yu-wei, DONG Pei-hong
Department of Infectious Disease,Wenzhou Central Hospital,Wenzhou,Zhejiang 325000,China
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摘要 目的 研究黄芩苷体内抑制结核分枝杆菌的作用机制,为耐药结核病治疗提供依据。方法 取40只雄性昆明小鼠,尾静脉注射耐异烟肼结核分枝杆菌构建动物模型,按不同治疗方法分别纳入结核组、异烟肼组、NF-κB抑制组和黄芩苷组,每组10只,建模后第8 d采集肺组织和心脏外周血,采用HE染色观察肺的形态变化,采用抗酸染色镱检和定量PCR法检测肺组织内结核分枝杆菌数,采用免疫组化检测肺组织中巨噬细胞数,采用流式细胞学检测单核/巨噬细胞NF-κB和TLR4的表达。结果 黄芩苷组小鼠体重高于结核组、异烟肼组和NF-κB抑制组(P<0.05);黄芩苷组小鼠单核/巨噬细胞NF-κB和TLR4平均荧光强度分别为448.21±30.61和401.01±34.58,均高于结核组和异烟肼组(P<0.05);结核组、异烟肼组和NF-κB抑制组均可观察到典型的结核慢性肉芽肿性病变,而黄芩苷组未见典型的结核病变;黄芩苷组小鼠肺组织内结核分枝杆菌数、CD68+巨噬细胞数均少于结核组、异烟肼组和NF-κB抑制组(P<0.05)。结论 黄芩苷可通过调控巨噬细胞NF-κB和TLR4的表达起到抗结核作用,但加用NF-κB抑制剂后会明显削弱黄芩苷的抗结核作用。
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赵丰权
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董培红
关键词 结核分枝杆菌黄芩苷巨噬细胞NF-κB;TLR4    
AbstractObjective To study the mechanism of baicalin in inhibiting Mycobacterium tuberculosis(MTB)and to provide reference for drug-resistant tuberculosis treatment. Methods Forty male Kunming mice were injected isoniazid-resistant MTB into their tail veins to build models of infection. They were evenly divided into MTB group,isophosiazone group,NF-κB inhibition group and baicalicin group according to treatment. The lung tissue and peripheral blood of the mice were collected on the 8th day after modeling. The morphological changes of the lungs were observed by HE staining. The number of MTB in lung tissue was detected by acid-fast staining and quantitative PCR. The number of macrophagein lung tissue was detected by immunohistochemistry. The expression of NF-κB and TLR4 in monocytes/macrophages were detected by flow cytometry. Results The average weight of mice in the baicalicin group was significantly higher than that in the MTB group,the isophosiazone group and the NF-κBinhibition group(P<0.05). The average fluorescence intensity of NF-κB and TLR4 in monocytes/macrophages in the baicalicin group were 448.21±30.61 and 401.01±34.58,which were significantly higher than those in the MTB group and the isophosiazone group(P<0.05). Typical tuberculous chronic granulomatous lesions were observed in the MTB group,isophosiazone group and NF-κB inhibition group,except the baicalin group. The mean number of MTB and CD68+ macrophagesin lung tissue of mice in the baicalin group were significantly less than that in the MTB group,the isophosiazone group and the NF-κB inhibition group(P<0.05). Conclusion Baicalin achieves an anti-tuberculosis effect by regulating the expression of NF-κB and TLR4 in macrophages,which can be weakened by adding NF-κB inhibitor.
Key wordsMycobacterium tuberculosis    Baicalin    Macrophage    NF-κB;    TLR4
收稿日期: 2019-02-19      出版日期: 2019-09-26
ZTFLH:  R285  
通信作者: 赵丰权,E-mail:zzzouu@yeah.net   
作者简介: 赵丰权,本科,医师,主要从事肺结核、肝炎和艾滋病等感染性疾病的临床和基础研究工作
引用本文:   
赵丰权, 戴建义, 李君桦, 蔡玉伟, 董培红. 黄芩苷体内抑制结核分枝杆菌的机制研究[J]. 预防医学, 2019, 31(10): 998-1001.
ZHAO Feng-quan, DAI Jian-yi, LI Jun-hua, CAI Yu-wei, DONG Pei-hong. Baicalin inhibit Mycobacterium tuberculosis in vivo by regulating the expression of Toll like receptor 4 and nuclear factor κB. Preventive Medicine, 2019, 31(10): 998-1001.
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http://www.zjyfyxzz.com/CN/10.19485/j.cnki.issn2096-5087.2019.10.006      或      http://www.zjyfyxzz.com/CN/Y2019/V31/I10/998
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