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In vitro and in vivo study demonstrates arginine enhances florfenicol’s antibacterial efficacy, indicating a novel drug combination approach.
both in vivo and in vitro, successfully reversing the resistance phenotype. Mechanistic studies reveal that Arg disrupts fatty acid β-oxidation by inhibiting the arginine succinyl-transferase (AST) pathway, leading to excessive free fatty acid (FFA) accumulation. This triggers membrane structural damage, energy metabolism disorders, and oxidative stress. Concurrently, Arg inhibits the expression and function of multidrug efflux pumps such as AcrAB-TolC and EmrAB-TolC, reducing FFC efflux and increasing its intracellular concentration. This study systematically reveals a novel pathway whereby Arg synergistically enhances the antibacterial activity of FFC through dual mechanisms of metabolic reprogramming and efflux pump inhibition, providing theoretical support for the development and application of amino acid compounds as antibiotic adjuvants.
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Cao et al. (2026) studied this question.
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