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. 2019 Nov 26:2019:1250645.
doi: 10.1155/2019/1250645. eCollection 2019.

Resistance Modulation Action, Time-Kill Kinetics Assay, and Inhibition of Biofilm Formation Effects of Plumbagin from Plumbago zeylanica Linn

Emmanuel B A Adusei  1 , Reimmel K Adosraku  1 , James Oppong-Kyekyeku  1 , Cedric D K Amengor  2 , Yakubu Jibira  3
Affiliations

Resistance Modulation Action, Time-Kill Kinetics Assay, and Inhibition of Biofilm Formation Effects of Plumbagin from Plumbago zeylanica Linn

Emmanuel B A Adusei et al. J Trop Med. .

Abstract

Antimicrobial resistance (AMR) is a threat to the prevention and treatment of the increasing range of infectious diseases. There is therefore the need for renewed efforts into antimicrobial discovery and development to combat the menace. The antimicrobial activity of plumbagin isolated from roots of Plumbago zeylanica against selected organisms was evaluated for resistance modulation antimicrobial assay, time-kill kinetics assay, and inhibition of biofilm formation. The minimum inhibitory concentrations (MICs) of plumbagin and standard drugs were determined via the broth microdilution method to be 0.5 to 8 μg/mL and 0.25-128 μg/mL, respectively. In the resistance modulation study, MICs of the standard drugs were redetermined in the presence of subinhibitory concentration of plumbagin (4 μg/mL), and plumbagin was found to either potentiate or reduce the activities of these standard drugs with the highest potentiation recorded up to 12-folds for ketoconazole against Candida albicans. Plumbagin was found to be bacteriostatic and fungistatic from the time-kill kinetics study. Plumbagin demonstrated strong inhibition of biofilm formation activity at concentrations of 128, 64, and 32 μg/mL against the test microorganisms compared with ciprofloxacin. Plumbagin has been proved through this study to be a suitable lead compound in antimicrobial resistance drug development.

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Conflict of interest statement

The authors declare that there are no conflicts of interest regarding the publication of this study.

Figures

Figure 1
Figure 1
Chemical structure of plumbagin.
Figure 2
Figure 2
Time-kill kinetics of plumbagin against Staphylococcus aureus. (a) Time-kill kinetics curve and (b) AUC of time-kill kinetics. AUC: area under the curve. n=3; values are mean ± SEM. ∗∗∗p < 0.0001 (one-way ANOVA followed by Dunnett's post hoc test).
Figure 3
Figure 3
Time-kill kinetics of plumbagin against Escherichia coli. (a) Time-kill kinetics curve and (b) AUC of time-kill kinetics. AUC: area under the curve. n=3; values are mean ± SEM. ∗∗∗p < 0.0001 (one-way ANOVA followed by Dunnett's post hoc test).
Figure 4
Figure 4
Time-kill kinetics of plumbagin against Pseudomonas aeruginosa. (a) Time-kill kinetics curve and (b) AUC of time-kill kinetics. AUC: area under the curve. n=3; values are mean ± SEM. ∗∗∗p < 0.0001 (one-way ANOVA followed by Dunnett's post hoc test).
Figure 5
Figure 5
Time-kill kinetics of plumbagin against Candida albicans. (a) Time-kill kinetics curve and (b) AUC of time-kill kinetics. AUC: area under the curve. n=3; values are mean ± SEM. ∗∗∗p < 0.0001 (one-way ANOVA followed by Dunnett's post hoc test).
Figure 6
Figure 6
Percentage inhibition effect of plumbagin and ciprofloxacin (positive control) on biofilm formation by biofilm forming organisms: (a) Staphylococcus aureus, (b) Escherichia coli, (c) Klebsiella pneumoniae, and (d) Pseudomonas aeruginosa.
See this image and copyright information in PMC

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