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Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo

Pseudorabies (PR) is an acute and severe infectious disease caused by pseudorabies virus (PRV). Once the virus infects pigs, it is difficult to eliminate, resulting in major economic losses to the global pig industry. In addition, reports of human infection with PRV suggest that the virus is a poten...

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Autores principales: Cai, Xiaojing, Wang, Zhiying, Li, Xiaocheng, Zhang, Jing, Ren, Zhiyuan, Shao, Yi, Xu, Yongkang, Zhu, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10537396/
https://www.ncbi.nlm.nih.gov/pubmed/37764342
http://dx.doi.org/10.3390/molecules28186567
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author Cai, Xiaojing
Wang, Zhiying
Li, Xiaocheng
Zhang, Jing
Ren, Zhiyuan
Shao, Yi
Xu, Yongkang
Zhu, Yan
author_facet Cai, Xiaojing
Wang, Zhiying
Li, Xiaocheng
Zhang, Jing
Ren, Zhiyuan
Shao, Yi
Xu, Yongkang
Zhu, Yan
author_sort Cai, Xiaojing
collection PubMed
description Pseudorabies (PR) is an acute and severe infectious disease caused by pseudorabies virus (PRV). Once the virus infects pigs, it is difficult to eliminate, resulting in major economic losses to the global pig industry. In addition, reports of human infection with PRV suggest that the virus is a potential threat to human health; thus, its significance to public health should be considered. In this paper, the anti-PRV activities of emodin in vitro and in vivo, and its mechanism of action were studied. The results showed that emodin inhibited the proliferation of PRV in PK15 cells in a dose-dependent manner, with an IC50 of 0.127 mg/mL and a selection index of 5.52. The addition of emodin at different stages of viral infection showed that emodin inhibited intracellular replication. Emodin significantly inhibited the expression of the IE180, EP0, UL29, UL44, US6, and UL27 genes of PRV within 48 h. Emodin also significantly inhibited the expression of PRV gB and gD proteins. The molecular docking results suggested that emodin might form hydrogen bonds with PRV gB and gD proteins and affect the structure of viral proteins. Emodin effectively inhibited the apoptosis induced by PRV infection. Moreover, emodin showed a good protective effect on PRV-infected mice. During the experimental period, all the control PRV-infected mice died resulting in a survival rate of 0%, while the survival rate of emodin-treated mice was 28.5%. Emodin also significantly inhibited the replication of PRV in the heart, liver, brain, kidneys and lungs of mice and alleviated tissue and organ damage caused by PRV infection. Emodin was able to combat viral infection by regulating the levels of the cytokines TNF-α, IFN-γ, IL-6, and IL-4 in the sera of infected mice. These results indicate that emodin has good anti-PRV activity in vitro and in vivo, and is expected to be a new agent for the prevention and control of PRV infection.
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spelling pubmed-105373962023-09-29 Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo Cai, Xiaojing Wang, Zhiying Li, Xiaocheng Zhang, Jing Ren, Zhiyuan Shao, Yi Xu, Yongkang Zhu, Yan Molecules Article Pseudorabies (PR) is an acute and severe infectious disease caused by pseudorabies virus (PRV). Once the virus infects pigs, it is difficult to eliminate, resulting in major economic losses to the global pig industry. In addition, reports of human infection with PRV suggest that the virus is a potential threat to human health; thus, its significance to public health should be considered. In this paper, the anti-PRV activities of emodin in vitro and in vivo, and its mechanism of action were studied. The results showed that emodin inhibited the proliferation of PRV in PK15 cells in a dose-dependent manner, with an IC50 of 0.127 mg/mL and a selection index of 5.52. The addition of emodin at different stages of viral infection showed that emodin inhibited intracellular replication. Emodin significantly inhibited the expression of the IE180, EP0, UL29, UL44, US6, and UL27 genes of PRV within 48 h. Emodin also significantly inhibited the expression of PRV gB and gD proteins. The molecular docking results suggested that emodin might form hydrogen bonds with PRV gB and gD proteins and affect the structure of viral proteins. Emodin effectively inhibited the apoptosis induced by PRV infection. Moreover, emodin showed a good protective effect on PRV-infected mice. During the experimental period, all the control PRV-infected mice died resulting in a survival rate of 0%, while the survival rate of emodin-treated mice was 28.5%. Emodin also significantly inhibited the replication of PRV in the heart, liver, brain, kidneys and lungs of mice and alleviated tissue and organ damage caused by PRV infection. Emodin was able to combat viral infection by regulating the levels of the cytokines TNF-α, IFN-γ, IL-6, and IL-4 in the sera of infected mice. These results indicate that emodin has good anti-PRV activity in vitro and in vivo, and is expected to be a new agent for the prevention and control of PRV infection. MDPI 2023-09-11 /pmc/articles/PMC10537396/ /pubmed/37764342 http://dx.doi.org/10.3390/molecules28186567 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Cai, Xiaojing
Wang, Zhiying
Li, Xiaocheng
Zhang, Jing
Ren, Zhiyuan
Shao, Yi
Xu, Yongkang
Zhu, Yan
Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title_full Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title_fullStr Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title_full_unstemmed Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title_short Emodin as an Inhibitor of PRV Infection In Vitro and In Vivo
title_sort emodin as an inhibitor of prv infection in vitro and in vivo
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10537396/
https://www.ncbi.nlm.nih.gov/pubmed/37764342
http://dx.doi.org/10.3390/molecules28186567
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