Dexamethasone inhibits SARS-CoV-2 spike pseudotyped virus viropexis by binding to ACE2

Copyright © 2020 Elsevier Inc. All rights reserved..

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 KD 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 ACE2h 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.

Media Type:

Electronic Article

Year of Publication:

2021

Contained In:

Virology - Vol. 554 (2021), p. 83-88

Language:

English

Contributors:

Zhang, Yongjing
Hu, Shiling
Wang, Jue
Xue, Zhuoyin
Wang, Cheng
Wang, Nan

Links:

Volltext

Keywords:

7S5I7G3JQL
ACE2
ACE2 protein, human
Angiotensin-Converting Enzyme 2
Binding Sites
Dexamethasone
EC 3.4.17.23
HEK293 Cells
Humans
Journal Article
Molecular Docking Simulation
Protein Binding
Research Support, Non-U.S. Gov't
SARS-CoV-2
Spike Glycoprotein, Coronavirus
Spike protein, SARS-CoV-2
Virus Internalization

Notes:

Date Completed 28.01.2021

Date Revised 28.01.2021

published: Print-Electronic

Citation Status MEDLINE

Copyright: From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Physical Description:

Online-Ressource

doi:

10.1016/j.virol.2020.12.001

PMID:

33387788

PPN (Catalogue-ID):

NLM320535142