ArticleBMC veterinary research2025
Andrographolide reverses the susceptibility of Streptococcus suis to aminoglycoside antibiotics by proton motive force.
Article in BMC veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Anti-Streptococcal Activity of β-Thujaplicin and Its Effect on Natural Low-Level Resistance ofPathogens (Basel, Switzerland) · 2026Article
- Antimicrobial Activity of Aurisin A AgainstInternational journal of molecular sciences · 2026Article
- Effects of Andrographolide-Loaded Nanostructured Lipid Carriers on Growth, Feed Efficiency, and Resistance toAnimals : an open access journal from MDPI · 2025Article
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7 authors.
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Abstract
backgroundThe global rise in multidrug-resistant bacteria has significantly undermined the efficacy of traditional antibiotics. Multidrug-resistant Streptococcus suis (S. suis), a pathogen capable of infecting pigs and humans, has been identified as a critical threat, causing severe meningitis and rapid mortality. In response, researchers have increasingly focused on herbal compounds as non-traditional antimicrobial agents, which can inhibit bacterial growth while minimizing the risk of resistance development. This study investigates the mechanism through which andrographolide (AP) restores the susceptibility of S. suis to aminoglycoside antibiotics.
methodsThe intracellular ΔpH in S. suis was assessed using the 2',7' -bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCCF-AM) probe to evaluate alterations in the proton motive force (PMF) following treatment with AP. Non-targeted metabolomics was employed to confirm changes in the metabolic profile of S. suis upon exposure to AP. Finally, an in vivo infection model was utilized to evaluate the therapeutic efficacy of AP in combination with antibiotics.
resultsExtensive in vitro experiments demonstrated that AP significantly enhances the activity of aminoglycoside antibiotics against diverse pathogens, including S. suis. Further studies revealed that bacterial death results from AP-mediated upregulation of the S. suis PMF, which enhances cellular uptake of tobramycin (TOB). Moreover, AP significantly upregulated pyruvate metabolism in S. suis, accelerated the tricarboxylic acid (TCA) cycle, and increased nicotinamide adenine dinucleotide (NADH) production. This metabolic shift further augmented the PMF. Combining AP with aminoglycoside antibiotics significantly reduced bacterial load and organ lesions in various organs in mice.
conclusionAP holds promise as an adjuvant to aminoglycoside antibiotics for combating S. suis-induced infections, offering a theoretical foundation for clinical applications.
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