Please wait a minute...
文章检索
预防医学  2019, Vol. 31 Issue (10): 998-1000,1006    DOI: 10.19485/j.cnki.issn2096-5087.2019.10.006
  论著 本期目录 | 过刊浏览 | 高级检索 |
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
全文: PDF(412 KB)  
输出: BibTeX | EndNote (RIS)      
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。
服务
把本文推荐给朋友
加入引用管理器
E-mail Alert
RSS
作者相关文章
赵丰权
戴建义
李君桦
蔡玉伟
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      修回日期: 2019-07-25     
中图分类号:  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): 998-1000,1006.
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): 998-1000,1006.
链接本文:  
http://www.zjyfyxzz.com/CN/10.19485/j.cnki.issn2096-5087.2019.10.006      或      http://www.zjyfyxzz.com/CN/Y2019/V31/I10/998
[1] MARAIS B J,SINTCHENKO V.Epidemic spread of multidrug-resistant tuberculosis in China[J]. Lancet Infectious Diseases,2017,17(3):238-239.
[2] SHAH N S,AULD S C,BRUST J C M,et al. Transmission of extensively drug-resistant tuberculosis in South Africa[J]. New England Journal of Medicine,2017,376(3):243.
[3] WANG P,CAO Y,YU J,et al.Baicalin alleviates ischemia-induced memory impairment by inhibiting the phosphorylation of CaMKII in hippocampus[J]. Brain Research,2016,1642:95-103.
[4] ZHU W,JIN Z,YU J,et al.Baicalin ameliorates experimental inflammatory bowel disease through polarization of macrophages to an M2 phenotype.[J]. International Immunopharmacology,2016, 35:119-126.
[5] LIU J,WEI Y,LUO Q,et al.Baicalin attenuates inflammation in mice with OVA-induced asthma by inhibiting NF-κB and suppressing CCR7/CCL19/CCL21[J]. International Journal of Molecular Medicine,2016,38(5):1541-1548.
[6] 吴正吉,张渝成,吴蕊鑫,等. 黄芩苷对耐多药结核鼠VEGF、MMP-9表达及对血清炎症因子的影响[J]. 中国地方病防治杂志,2016,31(3):339-340.
[7] 吴燕燕,王易,王莉新.黄芩苷对结核分枝杆菌作用下TLR2-MyD88信号通路的影响[J]. 中国免疫学杂志,2011, 27(8):714-717.
[8] 邵世峰,刘雪萍,孙婉蓉,等. 黄芩苷对结核分枝杆菌抑菌作用的初步研究[J]. 天津医药,2012,40(8):763-765.
[9] 王燕平,叶品良,张传涛,等. 肺痨康对耐异烟肼肺结核小鼠miRNA-29b和caspase-3的影响[J]. 中医药导报,2016,22(6):28-31.
[10] 陈忻,赵晖,张楠,等. 黄芩苷对小鼠免疫性肝损伤的保护作用[J]. 中药药理与临床,2006,22(3):39-40.
[11] 戴建义,苏菲菲,杨守峰,等. 复治结核病患者外周血淋巴细胞亚群变化及临床意义[J]. 上海预防医学,2014,26(4):180-181.
[12] 肖红侠,张喜霞,邵世峰,等. 黄芩苷对结核分枝杆菌抑菌作用的研究[J]. 临床检验杂志,2017,35(4):291-292.
[13] FU S,XU L,LI S,et al.Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B(NF-κB)signaling during Haemophilus parasuis infection[J]. Veterinary Research,2016, 47(1):80.
[14] LIU X,LIU C.Baicalin ameliorates chronic unpredictable mild stress-induced depressive behavior:Involving e inhibition of NLRP3 inflammasome activation in rat prefrontal cortex[J]. International Immunopharmacology,2017,48:30-34.
[15] HE X W,YU D,LI W L,et al.Anti-atherosclerotic potential of baicalin mediated by promoting cholesterol efflux from macrophages via the PPARγ-LXRα-ABCA1/ABCG1 pathway[J]. Biomedicine & Pharmacotherapy,2016,83:257-264.
[16] KUMAR R,SAHU S K,KUMAR M,et al.MicroRNA 17-5p regulates autophagy in Mycobacterium tuberculosis-infected macrophages by targeting Mcl-1 and STAT3[J]. Cellular Microbiology,2016, 18(5):679-691.
[17] KALAM H,FONTANA M F,KUMAR D.Alternate splicing of transcripts shape macrophage response to Mycobacterium tuberculosis infection[J]. Plos Pathogens,2017,13(3):e1006236.
[18] BOUTTIER M,LAPERRIERE D,MEMARI B,et al.Alu repeats as transcriptional regulatory platforms in macrophage responses to M.tuberculosis infection[J]. Nucleic Acids Research,2016,44(22):10571-10587.
[19] BERG R D,STEVEN L,O' SULLIVAN M P,et al. Lysosomal disorders drive susceptibility to tuberculosis by compromising macrophage migration[J]. Cell,2016,165(1):139-152.
[20] BRACE P T,TEZERA L B,BIELECKA M K,et al.Mycobacterium tuberculosis subverts negative regulatory pathways in human macrophages to driveimmunopathology[J]. Plos Pathogens,2017, 13(6):e1006367.
[1] 王远航, 胡洁, 葛锐, 富小飞, 亓云鹏. 嘉兴市结核分枝杆菌耐药情况分析[J]. 预防医学, 2023, 35(8): 705-709.
[2] 雷蓉蓉, 张婷, 吴成果, 罗建奎, 汪清雅, 任昌理. 南川区居民结核潜伏感染调查[J]. 预防医学, 2022, 34(4): 371-374.
[3] 纪律, 刘晓俊, 余云芳, 余枫华, 周攀. 宜昌市耐药结核分枝杆菌MIRU-VNTR分子特征及耐药基因突变分析[J]. 预防医学, 2021, 33(2): 149-152.
[4] 狄春红, 章云衡, 谭晓华, 杨磊. 砷对巨噬细胞胆固醇流出及ABCA1、ABCG1、SRBI基因表达的影响[J]. 预防医学, 2021, 33(10): 977-982.
[5] 叶静芬, 方晴, 胡耀仁, 许小敏, 车洋. 北京基因型耐多药结核分枝杆菌二线抗结核药物耐药基因突变特征分析[J]. 预防医学, 2021, 33(10): 983-987.
[6] 朱业蕾, 潘爱珍, 周琳, 柳正卫, 张明五, 吴坤阳, 王晓萌, 吴蓓蓓. 浙江省非结核分枝杆菌流行状况及耐药性分析[J]. 预防医学, 2021, 33(1): 6-10.
[7] 郭海萍, 尚媛媛, 李姗姗, 逄宇. 全基因组测序在结核病分子流行病学研究中的应用[J]. 预防医学, 2020, 32(9): 899-903.
[8] 王涧, 严丽英, 徐新美, 刘干红,沈惠良. 巨噬细胞在麻风免疫致病机制中的作用[J]. 预防医学, 2020, 32(5): 475-478.
[9] 高华强, 卢巧玲, 金法祥, 孟海滨, 孙佳美, 许树红. 绍兴市肺结核患者耐药特征分析[J]. 预防医学, 2020, 32(4): 384-387.
[10] 贾庆军, 谢立, 吴亦斐, 王乐, 陆敏, 赵刚. 杭州市结核病患者耐药检测结果分析[J]. 预防医学, 2019, 31(3): 289-292.
[11] 胡瑜洁, 姚晓霖, 钟涛. 血糖波动对糖尿病大鼠肝脏TLR4和TNF-α表达的影响[J]. 预防医学, 2019, 31(1): 15-19.
[12] 王静,刘立宾,岳永宁,张艳,陈园园,鲍志坚,蔡青山,朱敏. TB-SAT检测支气管肺泡灌洗液诊断肺结核的价值研究[J]. 预防医学, 2018, 30(4): 429-431.
[13] 周康, 张永为, 陆新建, 马春芳. 葫芦素B对脂多糖诱导小鼠肺泡巨噬细胞炎症反应的影响[J]. 预防医学, 2017, 29(7): 680-683,688.
[14] 吴祥兵, 李娜, 蔡明明, 唐少华. 应用Xpert MTB/RIF技术快速筛查耐多药肺结核[J]. 预防医学, 2017, 29(7): 754-756.
[15] 竺祖军,夏强,岳永宁,张颖,胡佳娜,朱敏. XpertMTB/RIF检测技术在骨关节结核诊断中的应用价值[J]. 预防医学, 2017, 29(3): 322-324.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed