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天麻素通过促进I型干扰素的产生来抑制病毒感染。

Gastrodin Inhibits Virus Infection by Promoting the Production of Type I Interferon.

作者信息

Zhou Yunlian, Li Mengyao, Lv Tingyi, Huang Meixia, Cheng Beilei, Zhang Yuanyuan, Zhu Jie

机构信息

Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.

Department of Clinical Laboratory, Zhejiang Hospital, Hangzhou, China.

出版信息

Front Pharmacol. 2021 Feb 19;11:608707. doi: 10.3389/fphar.2020.608707. eCollection 2020.

DOI:10.3389/fphar.2020.608707
PMID:33776755
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7990098/
Abstract

Type I interferon (IFN-I) plays a critical role in the antiviral immune response. However, viruses have developed different strategies to suppress the production of IFN-I for its own escape and amplification. Therefore, promoting the production of IFN-I is an effective strategy against virus infection. Gastrodin (GTD), a phenolic glucoside extracted from Blume, has been reported to play a protective role in some central nervous system -related diseases and is beneficial for the recovery of diseases by inhibiting inflammation. However, the effect of GTD on virus infection is largely unknown. Here we found GTD treatment increased the survival rate of mice infected with vesicular stomatitis virus (VSV) or herpes simplex virus-1 (HSV-1). The production of IFN-I was increased in GTD-treated mice or macrophages compared to the control group, during virus infection. Furthermore, the activation of interferon regulatory factor 3 (IRF3) was promoted by GTD in macrophages upon VSV and HSV-1 infection. Our results demonstrated that GTD could inhibit the VSV and HSV-1 infection by promoting the production of IFN-I in macrophages and might provide an effective strategy against virus infection.

摘要

I型干扰素(IFN-I)在抗病毒免疫反应中起关键作用。然而,病毒已发展出不同策略来抑制IFN-I的产生以实现自身逃逸和增殖。因此,促进IFN-I的产生是对抗病毒感染的有效策略。天麻素(GTD)是从天麻中提取的一种酚苷,据报道在一些中枢神经系统相关疾病中发挥保护作用,且通过抑制炎症对疾病恢复有益。然而,GTD对病毒感染的影响在很大程度上尚不清楚。在此我们发现,GTD处理提高了感染水疱性口炎病毒(VSV)或单纯疱疹病毒1型(HSV-1)小鼠的存活率。在病毒感染期间,与对照组相比,GTD处理的小鼠或巨噬细胞中IFN-I的产生增加。此外,在VSV和HSV-1感染后,GTD促进巨噬细胞中干扰素调节因子3(IRF3)的激活。我们的结果表明,GTD可通过促进巨噬细胞中IFN-I的产生来抑制VSV和HSV-1感染,并可能提供一种对抗病毒感染的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/6ce48c1e898e/fphar-11-608707-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/997e109d2af9/fphar-11-608707-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/e25af9bff6ba/fphar-11-608707-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/e18e3cf55659/fphar-11-608707-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/d34aa7ace055/fphar-11-608707-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/d49f6d68accc/fphar-11-608707-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/6ce48c1e898e/fphar-11-608707-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/997e109d2af9/fphar-11-608707-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/e25af9bff6ba/fphar-11-608707-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/e18e3cf55659/fphar-11-608707-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/d34aa7ace055/fphar-11-608707-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/d49f6d68accc/fphar-11-608707-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c9f/7990098/6ce48c1e898e/fphar-11-608707-g006.jpg

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