tetano
Editor, Senior Moderator
Sci Rep
. 2024 Sep 12;14(1):21318.
doi: 10.1038/s41598-024-71486-0. PEG-SeNPs as therapeutic agents inhibiting apoptosis and inflammation of cells infected with H1N1 influenza A virus
Min Guo[SUP] 1 [/SUP], Yu-Dan Ye[SUP] 1 [/SUP], Jian-Piao Cai[SUP] 2 [/SUP], Hai-Tong Xu[SUP] 1 [/SUP], Wei Wei[SUP] 1 [/SUP], Jia-Yu Sun[SUP] 1 [/SUP], Chen-Yang Wang[SUP] 1 [/SUP], Chang-Bing Wang[SUP] 1 [/SUP], Ying-Hua Li[SUP] 3 [/SUP], Bing Zhu[SUP] 4 [/SUP]
Affiliations
The rapid variation of influenza challenges vaccines and treatments, which makes an urgent task to develop the high-efficiency and low-toxicity new anti-influenza virus drugs. Selenium is one of the essential trace elements for the human body that possesses a good antiviral activity. In this study, we assessed anti-influenza A virus (H1N1) activity of polyethylene glycol (PEG)-modified gray selenium nanoparticles (PEG-SeNPs) on Madin-Darby Canine Kidney (MDCK) cells in vitro. CCK-8 assay showed that PEG-SeNPs had a protective effect on H1N1-infected MDCK cells. Moreover, PEG-SeNPs significantly reduced the mRNA level of H1N1. TUNEL-DAPI test showed that DNA damage reached a high level but effectively prevented after PEG-SeNPs treatment. Meanwhile, JC-1, Annexin V-FITC and cell cycle assay demonstrated the apoptosis induced by H1N1 was reduced greatly when treated with PEG-SeNPs. Furthermore, the downregulation of p-ATM, p-ATR and P53 protein, along with the upregualation of AKT protein indicated that PEG-SeNPs could inhibit H1N1-induced cell apoptosis through reactive oxygen species (ROS)-mediated related signaling pathways. Finally, Cytokine detection demonstrated PEG-SeNPs inhibited the production of pro-inflammatory factors after infection, including IL-1β, IL-5, IL-6, and TNF-α. To sum up, PEG-SeNPs might become a new potential anti-H1N1 influenza virus drug due to its antiviral and anti-inflammatory activity.
Keywords: Apoptosis; Cytokine; Influenza virus; PEG-SeNPs; Signaling pathways.
. 2024 Sep 12;14(1):21318.
doi: 10.1038/s41598-024-71486-0. PEG-SeNPs as therapeutic agents inhibiting apoptosis and inflammation of cells infected with H1N1 influenza A virus
Min Guo[SUP] 1 [/SUP], Yu-Dan Ye[SUP] 1 [/SUP], Jian-Piao Cai[SUP] 2 [/SUP], Hai-Tong Xu[SUP] 1 [/SUP], Wei Wei[SUP] 1 [/SUP], Jia-Yu Sun[SUP] 1 [/SUP], Chen-Yang Wang[SUP] 1 [/SUP], Chang-Bing Wang[SUP] 1 [/SUP], Ying-Hua Li[SUP] 3 [/SUP], Bing Zhu[SUP] 4 [/SUP]
Affiliations
- PMID: 39266597
- DOI: 10.1038/s41598-024-71486-0
The rapid variation of influenza challenges vaccines and treatments, which makes an urgent task to develop the high-efficiency and low-toxicity new anti-influenza virus drugs. Selenium is one of the essential trace elements for the human body that possesses a good antiviral activity. In this study, we assessed anti-influenza A virus (H1N1) activity of polyethylene glycol (PEG)-modified gray selenium nanoparticles (PEG-SeNPs) on Madin-Darby Canine Kidney (MDCK) cells in vitro. CCK-8 assay showed that PEG-SeNPs had a protective effect on H1N1-infected MDCK cells. Moreover, PEG-SeNPs significantly reduced the mRNA level of H1N1. TUNEL-DAPI test showed that DNA damage reached a high level but effectively prevented after PEG-SeNPs treatment. Meanwhile, JC-1, Annexin V-FITC and cell cycle assay demonstrated the apoptosis induced by H1N1 was reduced greatly when treated with PEG-SeNPs. Furthermore, the downregulation of p-ATM, p-ATR and P53 protein, along with the upregualation of AKT protein indicated that PEG-SeNPs could inhibit H1N1-induced cell apoptosis through reactive oxygen species (ROS)-mediated related signaling pathways. Finally, Cytokine detection demonstrated PEG-SeNPs inhibited the production of pro-inflammatory factors after infection, including IL-1β, IL-5, IL-6, and TNF-α. To sum up, PEG-SeNPs might become a new potential anti-H1N1 influenza virus drug due to its antiviral and anti-inflammatory activity.
Keywords: Apoptosis; Cytokine; Influenza virus; PEG-SeNPs; Signaling pathways.