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Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis

Chrysin has been proven to possess antiviral properties, but the precise underlying anti-influenza mechanism and its anti-influenza efficacy in vivo are largely unclear. In this study, we investigated the involvement of chrysin in the blockade of cell cycle and apoptosis in distinct cell lines subje...

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Autores principales: Liu, Ying, Song, Xun, Li, Chenyang, Hu, Hao, Li, Wanlin, Wang, Lu, Hu, Jing, Liao, Chenghui, Liang, Hanbai, He, Zhendan, Ye, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009290/
https://www.ncbi.nlm.nih.gov/pubmed/35432374
http://dx.doi.org/10.3389/fimmu.2022.872958
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author Liu, Ying
Song, Xun
Li, Chenyang
Hu, Hao
Li, Wanlin
Wang, Lu
Hu, Jing
Liao, Chenghui
Liang, Hanbai
He, Zhendan
Ye, Liang
author_facet Liu, Ying
Song, Xun
Li, Chenyang
Hu, Hao
Li, Wanlin
Wang, Lu
Hu, Jing
Liao, Chenghui
Liang, Hanbai
He, Zhendan
Ye, Liang
author_sort Liu, Ying
collection PubMed
description Chrysin has been proven to possess antiviral properties, but the precise underlying anti-influenza mechanism and its anti-influenza efficacy in vivo are largely unclear. In this study, we investigated the involvement of chrysin in the blockade of cell cycle and apoptosis in distinct cell lines subjected to two H1N1 influenza A virus (IAV) strains, as well as its anti-IAV activity in vivo. Here, we found an early unidentified finding that chrysin strongly impeded IAV replication through a mechanism that was autonomous of innate antiviral immune activation and viral protein interaction. Surprisingly, chrysin can suppress IAV-induced cell cycle arrest in the G0/G1 phase by downregulating the expression levels of P53 and P21 while promoting Cyclin D1/CDK4 and Cyclin E1/CDK2 activation. Furthermore, chrysin dramatically inhibited the IAV-triggered mitochondrial apoptotic pathway by altering the balance of Bax/Bcl-xl and reducing caspase-9 and caspase-3 activation. Accumulated reactive oxygen species (ROS) reduction may contribute to the inhibitory role of chrysin in cell cycle arrest and apoptosis following IAV infection. Notably, chrysin preferably inhibited IAV replication in the upper respiratory tract, indicating that it might be a promising drug for restraining the spread of respiratory viruses.
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spelling pubmed-90092902022-04-15 Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis Liu, Ying Song, Xun Li, Chenyang Hu, Hao Li, Wanlin Wang, Lu Hu, Jing Liao, Chenghui Liang, Hanbai He, Zhendan Ye, Liang Front Immunol Immunology Chrysin has been proven to possess antiviral properties, but the precise underlying anti-influenza mechanism and its anti-influenza efficacy in vivo are largely unclear. In this study, we investigated the involvement of chrysin in the blockade of cell cycle and apoptosis in distinct cell lines subjected to two H1N1 influenza A virus (IAV) strains, as well as its anti-IAV activity in vivo. Here, we found an early unidentified finding that chrysin strongly impeded IAV replication through a mechanism that was autonomous of innate antiviral immune activation and viral protein interaction. Surprisingly, chrysin can suppress IAV-induced cell cycle arrest in the G0/G1 phase by downregulating the expression levels of P53 and P21 while promoting Cyclin D1/CDK4 and Cyclin E1/CDK2 activation. Furthermore, chrysin dramatically inhibited the IAV-triggered mitochondrial apoptotic pathway by altering the balance of Bax/Bcl-xl and reducing caspase-9 and caspase-3 activation. Accumulated reactive oxygen species (ROS) reduction may contribute to the inhibitory role of chrysin in cell cycle arrest and apoptosis following IAV infection. Notably, chrysin preferably inhibited IAV replication in the upper respiratory tract, indicating that it might be a promising drug for restraining the spread of respiratory viruses. Frontiers Media S.A. 2022-03-31 /pmc/articles/PMC9009290/ /pubmed/35432374 http://dx.doi.org/10.3389/fimmu.2022.872958 Text en Copyright © 2022 Liu, Song, Li, Hu, Li, Wang, Hu, Liao, Liang, He and Ye https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Liu, Ying
Song, Xun
Li, Chenyang
Hu, Hao
Li, Wanlin
Wang, Lu
Hu, Jing
Liao, Chenghui
Liang, Hanbai
He, Zhendan
Ye, Liang
Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title_full Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title_fullStr Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title_full_unstemmed Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title_short Chrysin Ameliorates Influenza Virus Infection in the Upper Airways by Repressing Virus-Induced Cell Cycle Arrest and Mitochondria-Dependent Apoptosis
title_sort chrysin ameliorates influenza virus infection in the upper airways by repressing virus-induced cell cycle arrest and mitochondria-dependent apoptosis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009290/
https://www.ncbi.nlm.nih.gov/pubmed/35432374
http://dx.doi.org/10.3389/fimmu.2022.872958
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