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?:abstract
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The SARS-CoV-2 outbreak, began in late 2019, has caused a worldwide pandemic and shows no signs of slowing. Glucocorticoids (GCs), including dexamethasone (DEX), have been widely used as effective anti-inflammatory and immunosuppressant drugs. In this study, seven GCs had no obvious effect on cell viability of angiotensin converting enzyme 2 (ACE2) high expressed HEK293T cells when concentrations were under 10 μM. Molecular docking results revealed that DEX occupied with active binding site of ACE2 of SARS-CoV-2 spike protein. Surface plasmon resonance (SPR) results showed that K(D) value between DEX and ACE2 was (9.03 ± 0.78) e−6 M. Cell membrane chromatography (CMC) results uncovered that DEX had a chromatographic retention. DEX was found out to inhibiting the viropexis into ACE2(h) cells using SARS-CoV-2 spike pseudotyped virus. Therefore, DEX inhibits the entrance of SARS-CoV-2 spike pseudotyped virus into cell by binding to ACE2.
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?:doi
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10.1016/j.virol.2020.12.001
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document_parses/pdf_json/1d0926d40f45639af55f36e6e9b0cc0bfa69cd97.json
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document_parses/pmc_json/PMC7744032.xml.json
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?:title
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Dexamethasone inhibits SARS-CoV-2 spike pseudotyped virus viropexis by binding to ACE2
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