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10.1016/j.virol.2020.12.001

http://scihub22266oqcxt.onion/10.1016/j.virol.2020.12.001
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suck abstract from ncbi


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pmid33387788      Virology 2021 ; 554 (ä): 83-88
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  • Dexamethasone inhibits SARS-CoV-2 spike pseudotyped virus viropexis by binding to ACE2 #MMPMID33387788
  • Zhang Y; Hu S; Wang J; Xue Z; Wang C; Wang N
  • Virology 2021[Feb]; 554 (ä): 83-88 PMID33387788show ga
  • 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 muM. 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.
  • |Angiotensin-Converting Enzyme 2/chemistry/*metabolism[MESH]
  • |Binding Sites[MESH]
  • |Dexamethasone/metabolism/*pharmacology[MESH]
  • |HEK293 Cells[MESH]
  • |Humans[MESH]
  • |Molecular Docking Simulation[MESH]
  • |Protein Binding[MESH]
  • |SARS-CoV-2/*drug effects/metabolism/physiology[MESH]
  • |Spike Glycoprotein, Coronavirus/chemistry/*metabolism[MESH]


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