Bactericidal action of ginger (Zingiber officinale Roscoe) extract against Escherichia coli through synergistic modulation of the AcrAB-TolC efflux pump and inhibition of peptidoglycan synthesis: In vitro and in silico approaches

Article

作者: Moulick, Soumitra ; Bera, Rammohan ; Roy, Dijendra Nath

The emergence of multidrug-resistant Escherichia coli is considered a severe threat to global health, largely attributed to the bacterium's ability to expel antibiotics via efflux pump systems. This study explores the antibacterial efficacy of a methanol extract derived from Zingiber officinale R. (ginger), a traditional medicinal spice, against an E. coli strain overexpressing the AcrAB-TolC efflux system. To evaluate the extract's efficacy, three E. coli strains were tested: AG100 (AcrAB-TolC⁺), AG100A (ΔAcrAB), and D22 (lpxC mutant). The ginger extract exhibited antibacterial activity against E. coli AG100A and D22, with minimal inhibitory concentrations (MIC) and minimal bactericidal concentrations (MBC) of 625 μg/mL. However, the extract showed no inhibitory effect against E. coli AG100, even at 10 mg/mL, suggesting the AcrAB-TolC system plays a key role in resistance. Notably, combining the extract with an efflux pump inhibitor (EPI) strongly enhanced its bactericidal effect, reducing the MBC for AG100 to 313 μg/mL. EtBr accumulation assays confirmed that the ginger extract, in combination with EPI, amplified intracellular drug retention, peaking fluorescence within 30 min and sustaining elevated levels over 60 min. Molecular docking further revealed that bioactive compounds such as 6-shogaol strongly bind within the binding domain of AcrB homotrimer, inhibiting pump function. Additionally, cell wall biosynthesis assays demonstrated 69-75 % inhibition when the ginger extract was used at 2-fold-4-fold its MIC in the presence of EPI, further intensifying bactericidal effects. These results underscore ginger's dual-action mechanisms, highlighting its potential as an effective natural antimicrobial agent against drug-resistant E. coli.

2025-05-01·Neuroscience

6-shogaol alleviates excessive neuronal autophagy and calcium overload following cerebral ischemia–reperfusion injury by inhibiting the expression of DAPK1

Article

作者: Rao, Ouyang ; Zhu, Ning ; Zhou, Hangxiang ; Li, Yehong ; Liu, Ying ; Tao, Junling ; Li, Shixin

Cerebral ischemia-reperfusion injury (CIRI) is the primary pathological mechanism of ischemic stroke, leading to neuronal damage and triggering a series of pathological changes. This study investigates the neuroprotective effects and underlying mechanisms of 6-shogaol (6-SH) in CIRI. By establishing an in vitro OGD/R model and a rat cerebral ischemia-reperfusion model, we found that 6-SH significantly improved neuronal viability, alleviated pathological damage, and reduced autophagosome formation. Additionally, 6-SH treatment markedly inhibited the expression of DAPK1, decreased intracellular calcium ion concentration, and mitigated excessive autophagy. Mechanistic studies indicated that 6-SH reduces neuronal injury induced by CIRI by modulating DAPK1 phosphorylation and inhibiting its activity. This discovery provides a theoretical basis for considering 6-SH as a potential neuroprotective agent and offers new insights for clinical treatment of ischemic stroke.

2025-04-01·European Journal of Nutrition

6-Shogaol, a neuro-nutraceutical derived from ginger, alleviates motor symptoms and depression-like behaviors and modulates the release of monoamine neurotransmitters in Parkinson's disease mice

Article

作者: Cho, Jun-Young ; Lee, Seungmin ; Choi, Yujin ; Park, Boyoung Y ; Hong, Seon-Pyo ; Ju, In Gyoung ; Kim, Jin Se ; Eo, Hyeyoon ; Yoon, Hae-Jee ; Park, Hi-Joon ; Kim, Jin Hee ; Oh, Myung Sook

PURPOSEParkinson's disease (PD) disrupts the regulation of neurotransmitters in the brain, causing patients to experience not only motor symptoms but also non-motor symptoms such as depression. 6-shogaol (6S) is a potential neuro-nutraceutical derived from ginger, and is known to ameliorate motor symptoms by suppressing inflammation in PD mice. In this study, we investigated whether 6S can attenuate motor symptoms and depression-like behaviors through neurotransmitter regulation and to elucidate which neurotransmitters are intimately correlated with these effects.METHODSC57BL/6 J mice were injected with 30 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 5 d to induce PD. 6S was administered via oral gavage for 11 d, including the MPTP injection period.RESULTS6S alleviated MPTP-induced motor symptoms and depression-like behaviors. MPTP injection decreased the levels of seven neurotransmitters in the striatum and four neurotransmitters in the hippocampus. Administration of 6S increased striatal dopamine, serotonin, and norepinephrine levels and hippocampal dopamine, norepinephrine, serotonin, and γ-aminobutyric acid levels. Moreover, correlation analysis shown that the motor symptom improvement effect of 6S was associated with striatal dopamine, norepinephrine, serotonin, and 5-hydroxyindoleacetic acid levels. The effect of 6S on depressive-like behavior was significantly correlated with striatal dopamine metabolites and serotonin and hippocampal dopamine, norepinephrine, and serotonin. Immunohistochemistry showed that 6S upregulated the expression of the vesicular monoamine transporter 2, which was reduced by MPTP in the striatum and hippocampus.CONCLUSIONThis study demonstrated that 6S improved motor symptoms and depression-like behaviors by regulating the release of monoamine neurotransmitters.

100 项与 6-Shogaol 相关的药物交易

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