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Inhibition of H1N1 influenza virus-induced apoptosis by functionalized selenium nanoparticles with amantadine through ROS-mediated AKT signaling pathw

tetano

Editor, Senior Moderator
Int J Nanomedicine. 2018 Apr 3;13:2005-2016. doi: 10.2147/IJN.S155994. eCollection 2018.
[h=1]Inhibition of H1N1 influenza virus-induced apoptosis by functionalized selenium nanoparticles with amantadine through ROS-mediated AKT signaling pathways.[/h] Li Y[SUP]#[/SUP][SUP]1[/SUP], Lin Z[SUP]#[/SUP][SUP]1[/SUP], Guo M[SUP]1[/SUP], Zhao M[SUP]1[/SUP], Xia Y[SUP]1[/SUP], Wang C[SUP]1[/SUP], Xu T[SUP]1[/SUP], Zhu B[SUP]1[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] [h=4]Introduction:[/h] As a therapeutic antiviral agent, the clinical application of amantadine (AM) is limited by the emergence of drug-resistant viruses. To overcome the drug-resistant viruses and meet the growing demand of clinical diagnosis, the use of biological nanoparticles (NPs) has increased in order to develop novel anti-influenza drugs. The antiviral activity of selenium NPs with low toxicity and excellent activities has attracted increasing attention for biomedical intervention in recent years.
[h=4]Methods and results:[/h] In the present study, surface decoration of selenium NPs by AM (Se@AM) was designed to reverse drug resistance caused by influenza virus infection. Se@ AM with less toxicity remarkably inhibited the ability of H1N1 influenza to infect host cells through suppression of the neuraminidase activity. Moreover, Se@AM could prevent H1N1 from infecting Madin Darby Canine Kidney cell line and causing cell apoptosis supported by DNA fragmentation and chromatin condensation. Furthermore, Se@AM obviously inhibited the generation of reactive oxygen species and activation of phosphorylation of AKT.
[h=4]Conclusion:[/h] These results demonstrate that Se@AM is a potentially efficient antiviral pharmaceutical agent for H1N1 influenza virus.


[h=4]KEYWORDS:[/h] amantadine; apoptosis; influenza virus; nanodrug; selenium nanoparticles

PMID: 29662313 PMCID: PMC5892959 DOI: 10.2147/IJN.S155994
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