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 |
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| Year of Publication: |
2021 |
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| Contained In: |
Virology - Vol. 554 (2021), p. 83-88 |
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| Language: |
English |
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| Contributors: |
Zhang, Yongjing |
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| Links: |
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| 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 |
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| Physical Description: |
Online-Ressource |
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| doi: |
10.1016/j.virol.2020.12.001 |
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| PMID: |
33387788 |
| PPN (Catalogue-ID): |
NLM320535142 |
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| 520 | |a Copyright © 2020 Elsevier Inc. All rights reserved. | ||
| 520 | |a 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 | ||
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