ArticleACS omega2023
Inhibition of H3N2 Influenza Virus Induced Apoptosis by Selenium Nanoparticles with Chitosan through ROS-Mediated Signaling Pathways.
Article in ACS omega, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Selenium nanoparticles: Eco-friendly synthesis, biological activities and biomedical applications - A comprehensive review.Materials today. Bio · 2026Review
- Selenium-derived bioactive enablers for advanced therapies: From molecular redox modulation to broad-spectrum disease applications.Bioactive materials · 2026Review
- Antiviral activity of green synthesized selenium nanoparticles alone and in combination with chitosan against SARS-CoV-2.Discover nano · 2026Article
- Nanoparticle‑based antiviral strategies to combat the influenza virus (Review).Biomedical reports · 2024Review
- Selenium Nanoparticles Control H1N1 Virus by Inhibiting Inflammatory Response and Cell Apoptosis.Molecules (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, nanotechnology has received more and more attention in the antiviral field. Among them, selenium nanoparticles (SeNPs) have received a lot of attention. Chitosan, as a substance with antiviral effect, is limited by water solubility, low bioavailability, and poor stability. In this study, the combination of SeNPs with chitosan (Se@CS) showed less toxic and good anti-H3N2 infection effect. CCK-8 and RT-PCR showed that Se@CS effectively prevented H3N2 infection of MDCK cells by inhibiting viral replication and preventing cell fragmentation and cell aggregation. In addition, Se@CS can inhibit the excessive production of ROS and the change of mitochondrial membrane potential. More importantly, Se@CS can inhibit the late apoptosis of cells caused by virus, which may be related to the inhibition of apoptotic proteins in the ROS/JNK apoptotic signaling pathway. Finally, Se@CS was also found to inhibit H3N2-induced inflammation and alleviate infection. These results prove that Se@CS is a promising inhibitor for controlling influenza H3N2 virus infection.
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Registered trials
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