Emodin Successfully Inhibited Invasion of Brucella abortus Via Modulting Adherence, Microtubule Dynamics and ERK Signaling Pathway in RAW 264.7 Cells

The aim of this work is to investigate the protective efficacy of emodin, an active, naturallyoccurring anthraquinone derivative of several traditional Chinese herbs, against Brucella abortus infection in macrophages. Brucella were incubated with different concentrations of emodin and showed that ba...

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Veröffentlicht in:Journal of microbiology and biotechnology 2018-10, Vol.28 (10), p.1723-1729
Hauptverfasser: Huy, Tran Xuan Ngoc, Reyes, Alisha Wehdnesday Bernardo, Hop, Huynh Tan, Arayan, Lauren Togonon, Son, Vu Hai, Min, Wongi, Lee, Hu Jang, Kim, Suk
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Zusammenfassung:The aim of this work is to investigate the protective efficacy of emodin, an active, naturallyoccurring anthraquinone derivative of several traditional Chinese herbs, against Brucella abortus infection in macrophages. Brucella were incubated with different concentrations of emodin and showed that bacterial survival rates were markedly reduced in a dose-dependent manner at increasing incubation time points. Through bacterial infection assay, the highest non-cytotoxic concentration of emodin demonstrated attenuated invasion of Brucella into macrophages, however it did not inhibit the growth of these pathogens within the host cells. On the other hand, emodin effectively decreased the number of bacteria that adhered to host cells, which indicated its potential as an anti-adhesin agent. Furthermore, using immunoblotting and FACS assay for detecting MAPK signaling proteins and F-actin polymerization, respectively, the results showed that the emodin-incubated cells displayed modest reduction in the phosphorylation levels of ERK1/2 and inhibition of F-actin polymerization as compared to control cells. These findings indicate the potential use of emodin as a naturally-occurring alternative method for the prevention of animal brucellosis although this requires confirmation of safe clinical doses.
ISSN:1017-7825
1738-8872