■评估痰热清(TRQ)对肺炎克雷伯菌的体外和体内抗菌作用及其对细菌生物膜形成的抑制活性,探讨TRQ抑制肺炎克雷伯菌生物膜形成的作用机制。
■建立肺炎克雷伯菌体外生物膜模型,使用结晶紫染色和扫描电子显微镜(SEM)评估TRQ对生物膜形成的影响。此外,采用活板计数法评价TRQ对肺炎克雷伯菌生物膜的清除作用;采用q-RTPCR评价不同浓度TRQ对肺炎克雷伯菌生物膜相关基因表达的抑制作用;采用哈氏弧菌生物发光法检测群体感应信号分子AI-2的活性;建立肺炎克雷伯菌豚鼠肺部感染模型,在用药物治疗后,进行肺组织病理分析和肺组织细菌负荷测定。治疗组包括TRQ组,亚胺培南(IPM)组,TRQ+IPM组,无菌生理盐水组为对照组。
■通过TRQ体外实验显着抑制了肺炎克雷伯菌生物膜的形成。此外,当与IPM结合时,与TRQ组和单纯IPM组相比,生物膜中肺炎克雷伯菌的清除率显著增加.q-RTPCR分析显示,TRQ下调了肺炎克雷伯菌生物膜形成相关基因的表达,特别是luxS,wbbm,wzm,还有lsrK,并抑制细菌中AI-2分子的活性。体内实验证明TRQ能有效治疗豚鼠肺部感染,导致肺部炎症减少。此外,当与IPM结合时,肺组织中的细菌负荷显著减少.
■TRQ作为一种潜在的治疗药物,在肺炎克雷伯菌感染的治疗中起着巨大的作用,特别是与常规抗生素联合使用。TRQ可以通过抑制肺炎克雷伯菌生物膜的形成增强对细菌的清除作用,这为TRQ抗肺炎克雷伯菌感染的临床治疗提供了实验证据。
UNASSIGNED: To evaluate the antibacterial effect of Tanreqing (TRQ) against K. pneumoniae and its inhibition activity on bacterial biofilm formation in vitro and in vivo, and to explore the mechanism of the inhibitory effects of TRQ on K. pneumoniae biofilm formation.
UNASSIGNED: An in vitro biofilm model of K. pneumoniae was established, and the impact of TRQ on biofilm formation was evaluated using crystal violet staining and scanning electron microscopy (SEM). Furthermore, the clearance effect of TRQ against K. pneumoniae in the biofilm was assessed using the viable plate counting method; q-RT PCR was used to evaluate the inhibitory effect of different concentrations of TRQ on the expression of biofilm-related genes in Klebsiella pneumoniae; The activity of quorum sensing signal molecule AI-2 was detected by Vibrio harveyi bioluminescence assay; Meanwhile, a guinea pig lung infection model of Klebsiella pneumoniae was constructed, and after treated with drugs, pathological analysis of lung tissue and determination of bacterial load in lung tissue were performed. The treatment groups included TRQ group, imipenem(IPM) group, TRQ+IPM group, and sterile saline group as the control.
UNASSIGNED: The formation of K. pneumoniae biofilm was significantly inhibited by TRQ in vitro experiments. Furthermore, when combined with IPM, the clearance of K. pneumoniae in the biofilm was notably increased compared to the TRQ group and IPM group alone. q-RT PCR analysis revealed that TRQ down-regulated the expression of genes related to biofilm formation in K. pneumoniae, specifically luxS, wbbm, wzm, and lsrK, and also inhibited the activity of AI-2 molecules in the bacterium. In vivo experiments demonstrated that TRQ effectively treated guinea pig lung infections, resulting in reduced lung inflammation. Additionally, when combined with IPM, there was a significant reduction in the bacterial load in lung tissue.
UNASSIGNED: TRQ as a potential therapeutic agent plays a great role in the treatment of K. pneumoniae infections, particularly in combination with conventional antibiotics. And TRQ can enhanced the clearance effect on the bacterium by inhibiting the K. pneumoniae biofilm formation, which provided experimental evidence in support of clinical treatment of TRQ against K. pneumoniae infections.