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

被引:66
作者
Zhao, Xinghong [1 ]
Cui, Qiankun [1 ]
Fu, Qiuting [1 ]
Song, Xu [1 ]
Jia, Renyong [2 ]
Yang, Yi [1 ]
Zou, Yuanfeng [1 ]
Li, Lixia [1 ]
He, Changliang [1 ]
Liang, Xiaoxia [1 ]
Yin, Lizi [1 ]
Lin, Juchun [1 ]
Ye, Gang [1 ]
Shu, Gang [1 ]
Zhao, Ling [1 ]
Shi, Fei [1 ]
Lv, Cheng [1 ]
Yin, Zhongqiong [1 ]
机构
[1] Sichuan Agr Univ, Coll Vet Med, Nat Med Res Ctr, Chengdu 611130, Sichuan, Peoples R China
[2] Sichuan Agr Univ, Key Lab Anim Dis & Human Hlth Sichuan Prov, Chengdu 611130, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
HUMAN-IMMUNODEFICIENCY-VIRUS; ENDOTHELIN-1; GENE-EXPRESSION; BURKITTS-LYMPHOMA CELLS; REPLICATION; INFECTION; PROLIFERATION; LATENCY; TYPE-1;
D O I
10.1038/s41598-017-09365-0
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 mu M. 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-kappa B activation and NF-kappa B-dependent gene expression through its ability to inhibit I kappa B kinase activity, which is the key regulator in NF-kappa B 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 I kappa B kinase. These results provided a new alternative control measure for PRV infection and new insights into the antiviral mechanism of Res.
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页数:11
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