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

• Published in: International journal of nanomedicine 2018-01, Vol.13, p.2005-2016
• Main Authors: Li, Yinghua, Lin, Zhengfang, Guo, Min, Zhao, Mingqi, Xia, Yu, Wang, Changbing, Xu, Tiantian, Zhu, Bing
• Format: Article
• Language: English
• Subjects: Amantadine; Amantadine - administration & dosage; Amantadine - pharmacology; Animals; Antiviral Agents - administration & dosage; Antiviral Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Biomedical materials; Cancer; Cytotoxicity; Dogs; Drug Delivery Systems - methods; Drug resistance; Drug Resistance, Viral - drug effects; Hepatitis; Infections; Influenza A Virus, H1N1 Subtype - drug effects; Influenza A Virus, H1N1 Subtype - pathogenicity; Influenza virus; Laboratories; Madin Darby Canine Kidney Cells; Mutation; Nanoparticles; Nanoparticles - administration & dosage; Nanoparticles - chemistry; Original Research; Orthomyxoviridae Infections - drug therapy; Orthomyxoviridae Infections - virology; Peptides; Proteins; Proto-Oncogene Proteins c-akt - metabolism; Reactive oxygen species; Reactive Oxygen Species - metabolism; Selenium; Selenium - administration & dosage; Selenium - pharmacology; Selenium nanoparticles; Silver; Spectrum analysis; Swine flu; Viral infections; Viruses
• ISSN: 1178-2013; 1176-9114; 1178-2013
• DOI: 10.2147/IJN.S155994

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