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

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

    Int J Nanomedicine. 2018 Apr 3;13:2005-2016. doi: 10.2147/IJN.S155994. eCollection 2018.
    Inhibition of H1N1 influenza virus-induced apoptosis by functionalized selenium nanoparticles with amantadine through ROS-mediated AKT signaling pathways.

    Li Y#1, Lin Z#1, Guo M1, Zhao M1, Xia Y1, Wang C1, Xu T1, Zhu B1.
    Author information

    Abstract

    Introduction:

    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.
    Methods and results:

    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.
    Conclusion:

    These results demonstrate that Se@AM is a potentially efficient antiviral pharmaceutical agent for H1N1 influenza virus.


    KEYWORDS:

    amantadine; apoptosis; influenza virus; nanodrug; selenium nanoparticles

    PMID: 29662313 PMCID: PMC5892959 DOI: 10.2147/IJN.S155994
    Free PMC Article
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