The Inhibition of H1N1 Influenza Virus-Induced Apoptosis by Surface Decoration of Selenium Nanoparticles with β-Thujaplicin through Reactive Oxygen Species-Mediated AKT and p53 Signaling Pathways

beta-Thujaplicin possess a variety of biological activities. The use of modified biological nanoparticles (NPs) to develop novel anti-influenza drugs has increased in recent years. Selenium nanoparticles (SeNPs) with antiviral activity have attracted increasing attention for biomedical intervention. Functionalized SeNPs by beta-thujaplicin (Se@TP) surface modified with superior antiviral activity were synthesized in this study. Compared to a virus group (43%), when treated with Se@TP (88%), the cell survival rate of MDCK cells was 45% higher. Se@TP could inhibit H1N1 from infecting Madin-Darby canine kidney (MDCK) cells and block chromatin condensation and DNA fragmentation. Se@TP obviously prevented MDCK cells from generating reactive oxygen species. Furthermore, Se@TP prevents lung injury in H1N1-infected mice through eosin staining and hematoxylin in vivo. Mechanistic investigation revealed that Se@TP inhibited H1N1 influenza virus from infecting MDCK cells through induction of apoptosis via suppressing AKT and p53 signaling pathways through immunohistochemical assay. Our results suggest that beta-thujaplicin-modified SeNPs as carriers are an efficient way to achieve an antiviral pharmaceutical candidate for H1N1 influenza.