Study on the Mechanism of Coenzyme Q0 in Enhancing the Aminoglycoside Antibiotic Killing of Escherichia Coli

WANG Zi-han; CHEN Jia-jun; WANG Yu-chan; HUANG Di-hui

doi:10.13651/j.cnki.fjnykj.2025.10.010

Abstract：In order to further explore the functional characteristics and potential molecular mechanisms of Coenzyme Q0 as an antibiotic adjuvant,Escherichia coli BW25113 was used as the research object,and four treatment groups were set up:the blank group(Control),the gentamicin-treated group(Genta),the Coenzyme Q0-treated group(Q0),and the combined treatment group(Q0+Genta).The final concentration of gentamicin in the treated groups was 100 µg·mL-1,and the final concentration of Coenzyme Q0 was 30 µg·mL-1.Meanwhile,the hydrogen peroxide(30%solution)was used as the positive control for the determination of reactive oxygen species(ROS).The flow cytometry was employed to detect the intracellular ROS level and proton motive force(PMF)level;the cell membrane damage was evaluated by propidium iodide(PI)staining combined with the fluorescence microscopy;and the cell morphology was observed by using the scanning electron microscopy.The results showed that:Coenzyme Q0 could significantly affect the intracellular ROS level of bacteria,and its combination with antibiotics could generate more ROS,inducing bacteria to enter the state of oxidative stress.Coenzyme Q0 could disrupt the normal intracellular energy metabolism of bacteria,thereby reducing their PMF level.The results of outer membrane staining showed that the fluorescence intensity of bacteria in the combined treatment group was significantly higher than that in the single-treatment group,indicating that Coenzyme Q0 could damage the outer membrane of bacteria and thus increase the uptake of antibiotics.The results of scanning electron microscopy revealed that the integrity of bacterial membrane morphology in the combined treatment group was disrupted,which further enhanced the bactericidal effect of antibiotics.This study clarified the mechanism of Coenzyme Q0 enhancing the antibiotic bactericidal activity by regulating ROS,PMF and cell membrane structure,which provided a theoretical basis for its subsequent development.