ArticleBMC microbiology2025
Notoginsenoside Ft1 enhances the effectiveness of gentamicin against Escherichia coli by interfering with intrinsic antibacterial mechanisms.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundE. coli is a versatile human commensal bacterium and pathogen that can cause a variety of community-acquired and hospital-acquired infections. Gentamicin is an antibiotic commonly used in clinical settings to treat severe infections caused by E. coli; however, the emergence of resistant pathogens highlights the urgent need for alternative strategies to address this global burden.
resultsIn this study, we demonstrate that Notoginsenoside Ft1 can prevent the evolution of Gentamicin resistance in E. coli, restore the antibiotic’s efficacy against cells exposed to the antibiotic, and inhibit biofilm formation. Notably, Notoginsenoside Ft1 works in synergy with Gentamicin by interacting with active residues of the AcrAB-TolC efflux pump and dissipating the proton motive force (PMF), thereby disrupting the function of the AcrAB-TolC efflux pump and triggering a vicious cycle that compromises cell membrane integrity and disrupts metabolic homeostasis. Furthermore, various host infection models have demonstrated that the synergistic effects of the two compounds also exhibit significant efficacy in vivo.
conclusionsNotoginsenoside Ft1 serves as an effective adjuvant to Gentamicin and can be used in combination to treat infections caused by AcrAB-TolC positive pathogens. This study provides proof of concept and a starting point for investigating the molecular mechanisms by which Notoginsenoside Ft1 inhibits bacterial efflux pumps. These findings reveal the potential of Notoginsenoside Ft1 as a novel adjuvant to Gentamicin in combating infections caused by highly virulent E. coli.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.