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 | Zendy

Changbing Wang | Zendy; Haiyang Chen | Zendy; Danyang Chen | Zendy; Mingqi Zhao | Zendy; Zhengfang Lin | Zendy; Min Guo | Zendy; Tiantian Xu | Zendy; Yi Chen | Zendy; Liang Hua | Zendy; Tao Lin | Zendy; Ying Tang | Zendy; Bing Zhu | Zendy; Yinghua Li | Zendy

Open Access

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

Author(s) -

Changbing Wang,

Haiyang Chen,

Danyang Chen,

Mingqi Zhao,

Zhengfang Lin,

Min Guo,

Tiantian Xu,

Yi Chen,

Liang Hua,

Tao Lin,

Ying Tang,

Bing Zhu,

Yinghua Li

Publication year - 2020

Publication title -

acs omega

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.779

H-Index - 40

ISSN - 2470-1343

DOI - 10.1021/acsomega.0c04624

Subject(s) - apoptosis , influenza a virus , reactive oxygen species , in vivo , virus , dna fragmentation , protein kinase b , chemistry , selenium , fragmentation (computing) , signal transduction , biology , programmed cell death , biochemistry , virology , ecology , microbiology and biotechnology , organic chemistry

β-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 β-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 β-thujaplicin-modified SeNPs as carriers are an efficient way to achieve an antiviral pharmaceutical candidate for H1N1 influenza.

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