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白藜芦醇对伪狂犬病毒的抗病毒特性与其抑制 IκB 激酶激活有关。

Antiviral properties of resveratrol against pseudorabies virus are associated with the inhibition of IκB kinase activation.

机构信息

Natural Medicine Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, China.

Key laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China.

出版信息

Sci Rep. 2017 Aug 18;7(1):8782. doi: 10.1038/s41598-017-09365-0.

DOI:10.1038/s41598-017-09365-0
PMID:28821840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5562710/
Abstract

Pseudorabies virus (PRV) is a pathogen of swine resulting in devastating disease and economic losses worldwide. Resveratrol (Res) exhibits inhibitory activity against a wide range of viruses. Despite these important advances, the molecular mechanism(s) by which Res exerts its broad biological effects have not yet been elucidated. In this paper, the antiviral activity of Res against PRV and its mechanism of action were investigated. The results showed that Res potently inhibited PRV replication in a dose-dependent manner, with a 50% inhibition concentration of 17.17 μM. The inhibition of virus multiplication in the presence of Res was not attributed to direct inactivation or inhibition of viral entry into the host cells but to the inhibition of viral multiplication in host cells. Further studies demonstrated that Res is a potent inhibitor of both NF-κB activation and NF-κB-dependent gene expression through its ability to inhibit IκB kinase activity, which is the key regulator in NF-κB activation. Thus, the inhibitory effect of Res on PRV-induced cell death and gene expression may be due to its ability to inhibit the degradation of IκB kinase. These results provided a new alternative control measure for PRV infection and new insights into the antiviral mechanism of Res.

摘要

伪狂犬病毒(PRV)是一种猪病原体,可导致全球范围内毁灭性的疾病和经济损失。白藜芦醇(Res)对多种病毒具有抑制活性。尽管取得了这些重要进展,但 Res 发挥其广泛生物学作用的分子机制尚未阐明。本文研究了 Res 对 PRV 的抗病毒活性及其作用机制。结果表明,Res 能够以剂量依赖性方式强烈抑制 PRV 的复制,其 50%抑制浓度为 17.17 μM。Res 存在时抑制病毒繁殖不是归因于病毒直接失活或进入宿主细胞的抑制,而是归因于宿主细胞中病毒繁殖的抑制。进一步的研究表明,Res 通过抑制 IκB 激酶活性,是一种有效的 NF-κB 激活和 NF-κB 依赖性基因表达的抑制剂,IκB 激酶活性是 NF-κB 激活的关键调节因子。因此,Res 对 PRV 诱导的细胞死亡和基因表达的抑制作用可能是由于其抑制 IκB 激酶降解的能力。这些结果为 PRV 感染提供了新的替代控制措施,并深入了解了 Res 的抗病毒机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/9e9fc94f3c9c/41598_2017_9365_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/c04aede66a46/41598_2017_9365_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/305e5a4a6ee4/41598_2017_9365_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/038efd74b760/41598_2017_9365_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/c7716a0cf4df/41598_2017_9365_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/7b01a026bfbd/41598_2017_9365_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/94fadcb446ee/41598_2017_9365_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/9e9fc94f3c9c/41598_2017_9365_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/c04aede66a46/41598_2017_9365_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/305e5a4a6ee4/41598_2017_9365_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/038efd74b760/41598_2017_9365_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/c7716a0cf4df/41598_2017_9365_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/7b01a026bfbd/41598_2017_9365_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/94fadcb446ee/41598_2017_9365_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f178/5562710/9e9fc94f3c9c/41598_2017_9365_Fig7_HTML.jpg

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