首页|黄连素抑制肺炎克雷伯菌生物膜形成作用机制研究

黄连素抑制肺炎克雷伯菌生物膜形成作用机制研究

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目的 探讨黄连素对肺炎克雷伯菌(Klebsiella pneumoniae,KP)生物膜形成的作用,为KP相关感染的诊疗提供理论依据。方法 结晶紫半定量法观察不同浓度黄连素对KP生物膜形成过程的影响;实时荧光定量多聚核苷酸链式反应(RT-PCR)法检测1/8最低抑菌浓度(MIC)、1/4 MIC、1/2 MIC黄连素对KP的Ⅰ型和Ⅲ型菌毛fimA、fimH、mrkA、mrkD、fimK、mrkH基因表达的调控作用。结果 与对照组相比,黄连素组生物膜总量随黄连素浓度的增加而明显降低,差异有统计学意义(P<0。05);与对照组相比,黄连素组fimA、fimH、mrkA、mrkD、fimK、mrkH基因的表达水平均显著降低(P<0。05)。结论 黄连素有效抑制KP生物膜的形成与下调KP的Ⅰ型和Ⅲ型菌毛结构基因fimA、fimH、mrkA、mrkD以及调控基因fimK、mrkH的表达有关。
Research on the mechanism of Berberine inhibiting the formation of Klebsiella pneumoniae biofilm
Objective To investigate the effect of Berberine on the biofilm formation of Klebsiella pneumoniae(KP),and provide theoretical basis for the diagnosis and treatment of KP related infections.Methods The effect of Berberine on KP biofilm formation was observed by crystal violet semi-quantitative method.The expression of typeⅠ and type Ⅲ FIMi structural genes fimA,fimH,mrkA,mrkD and regulatory genes fimK and mrkH in KP detected by RT-PCR at 1/8MIC,1/4MIC and 1/2MIC doses.Results Compared with the control group,the total amount of biofilm in berberine group decreased significantly with increasing concentration,and the difference was statistically significant(P<0.05).Compared with the control group,the expression levels of fimA,fimH,mrkA,mrkD,fimK and mrkH genes in berberine group were significantly decreased(P<0.05).Conclusion Berberine effectively inhibits KP biofilm formation by down-regulating typeⅠand typeⅢFIMi structural genes fimA,fimH,mrkA,mrkD and regulatory genes fimK and mrkH.

BerberineKlebsiella pneumoniaeBiofilmFimbriae

刘冬梅、郭梦雨、费冰、李永伟、刘莹、任彦颖、刘心伟

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河南省中医院检验中心,河南 郑州 450002

河南中医药大学第二临床医学院,河南 郑州 450046

黄连素 肺炎克雷伯菌 生物膜 菌毛

国家中医临床研究基地科研专项

2021JDZX2075

2024

中国现代医药杂志
北京航天总医院

中国现代医药杂志

影响因子:0.689
ISSN:1672-9463
年,卷(期):2024.26(1)
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