Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis
Pseudorabies virus (PRV) infections have caused huge economic losses to the breeding industry worldwide, especially pig husbandry. PRV could threaten human health as an easily ignored zoonotic pathogen. The emergence of new mutants significantly reduced the protective effect of vaccination, indicati...
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MDPI AG
2023-02-01
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author | Xufan Zhao Yaqin Chen Wenrui Zhang Hui Zhang Yilong Hu Fengyu Yang Yingying Zhang Xu Song |
author_facet | Xufan Zhao Yaqin Chen Wenrui Zhang Hui Zhang Yilong Hu Fengyu Yang Yingying Zhang Xu Song |
author_sort | Xufan Zhao |
collection | DOAJ |
description | Pseudorabies virus (PRV) infections have caused huge economic losses to the breeding industry worldwide, especially pig husbandry. PRV could threaten human health as an easily ignored zoonotic pathogen. The emergence of new mutants significantly reduced the protective effect of vaccination, indicating an urgent need to develop specific therapeutic drugs for PRV infection. In this study, we found that dihydromyricetin (DMY) could dose-dependently restrain PRV infection in vitro with an IC50 of 161.34 μM; the inhibition rate of DMY at a concentration of 500 μM was 92.16 %. Moreover, the mode of action showed that DMY directly inactivated PRV virion and inhibited viral adsorption and cellular replication. DMY treatment could improve PRV-induced abnormal changes of the NF-κB signaling pathway and excessive inflammatory response through regulation of the contents of IκBα and p-P65/P65 and the transcriptional levels of cytokines (TNF-α, IL-1β and IL-6). Furthermore, DMY promoted the apoptosis of PRV-infected cells through the regulation of the expressions of Bax and Bcl-xl and the transcriptional levels of Caspase-3, Bax, Bcl-2 and Bcl-xl, thereby limiting the production of progeny virus. These findings indicated that DMY could be a candidate drug for the treatment of PRV infection. |
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spelling | doaj.art-6af4106f1d4b413db09b7ec14ca055d12023-11-16T23:45:47ZengMDPI AGVeterinary Sciences2306-73812023-02-0110211110.3390/vetsci10020111Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and ApoptosisXufan Zhao0Yaqin Chen1Wenrui Zhang2Hui Zhang3Yilong Hu4Fengyu Yang5Yingying Zhang6Xu Song7Natural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaCollege of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, ChinaNatural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, ChinaPseudorabies virus (PRV) infections have caused huge economic losses to the breeding industry worldwide, especially pig husbandry. PRV could threaten human health as an easily ignored zoonotic pathogen. The emergence of new mutants significantly reduced the protective effect of vaccination, indicating an urgent need to develop specific therapeutic drugs for PRV infection. In this study, we found that dihydromyricetin (DMY) could dose-dependently restrain PRV infection in vitro with an IC50 of 161.34 μM; the inhibition rate of DMY at a concentration of 500 μM was 92.16 %. Moreover, the mode of action showed that DMY directly inactivated PRV virion and inhibited viral adsorption and cellular replication. DMY treatment could improve PRV-induced abnormal changes of the NF-κB signaling pathway and excessive inflammatory response through regulation of the contents of IκBα and p-P65/P65 and the transcriptional levels of cytokines (TNF-α, IL-1β and IL-6). Furthermore, DMY promoted the apoptosis of PRV-infected cells through the regulation of the expressions of Bax and Bcl-xl and the transcriptional levels of Caspase-3, Bax, Bcl-2 and Bcl-xl, thereby limiting the production of progeny virus. These findings indicated that DMY could be a candidate drug for the treatment of PRV infection.https://www.mdpi.com/2306-7381/10/2/111pseudorabies virusdihydromyricetinantiviral activity |
spellingShingle | Xufan Zhao Yaqin Chen Wenrui Zhang Hui Zhang Yilong Hu Fengyu Yang Yingying Zhang Xu Song Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis Veterinary Sciences pseudorabies virus dihydromyricetin antiviral activity |
title | Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis |
title_full | Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis |
title_fullStr | Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis |
title_full_unstemmed | Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis |
title_short | Dihydromyricetin Inhibits Pseudorabies Virus Multiplication In Vitro by Regulating NF-κB Signaling Pathway and Apoptosis |
title_sort | dihydromyricetin inhibits pseudorabies virus multiplication in vitro by regulating nf κb signaling pathway and apoptosis |
topic | pseudorabies virus dihydromyricetin antiviral activity |
url | https://www.mdpi.com/2306-7381/10/2/111 |
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