This article is a Preprint
Preprints are preliminary research reports that have not been certified by peer review. They should not be relied on to guide clinical practice or health-related behavior and should not be reported in news media as established information.
Preprints posted online allow authors to receive rapid feedback and the entire scientific community can appraise the work for themselves and respond appropriately. Those comments are posted alongside the preprints for anyone to read them and serve as a post publication assessment.
Study on β-Chitosan against the binding of SARS-CoV-2S-RBD/ACE2 (preprint)
biorxiv; 2020.
Preprint
in English
| bioRxiv | ID: ppzbmed-10.1101.2020.07.31.229781
ABSTRACT
It has been known that SARS-CoV-2 which is considered similar to SARS-CoV invades human respiratory epithelial cells through interaction with the human angiotensin converting enzyme II (ACE2). In this work, SARS-CoV-2S-RBD and its cell receptor ACE2 were used to investigate the blocking effect and mechanism of {beta}-chitosan to the binding of them. Besides, inhibitory effect of {beta}-chitosan on inflammation induced by SARS-CoV-2S-RBD was also studied. Firstly, Native-PAGE results showed that {beta}-chitosan could bind with ACE2 or SARS-CoV-2S-RBD and the conjugate of {beta}-chitosan and ACE2 could no longer bind with SARS-CoV-2S-RBD. HPLC analyses suggested that was found the conjugate of {beta}-chitosan and SARS-CoV-2S-RBD displayed high binding affinity under the condition of high pressure (40 MPa) compared with that of ACE2 and SARS-CoV-2S-RBD. Furthermore, immunofluorescence detections on Vero E6 cells and hACE2 mice showed that {beta}-chitosan had a significant prevention and treatment effect on SARS-CoV-2S-RBD binding. Meanwhile, SARS-CoV-2S-RBD binding could activate the inflammation signaling pathways of cells and mice, however, {beta}-chitosan could dramatically suppress the inflammations activated by SARS-CoV-2S-RBD. Subsequently, Western blot analyses revealed that the expression levels of ACE2 in experimental groups treated with {beta}-chitosan significantly reduced. However, after the intervention of ADAM17 inhibitor (TAPI), the decreased ACE2 expressions affected by {beta}-chitosan up-regulated correspondingly. The results indicated that {beta}-chitosan has a similar antibody function, which can neutralize SARS-CoV-2S-RBD and effectively block the binding of SARS-CoV-2S-RBD with ACE2. ADAM17 activated by {beta}-chitosan can enhance the cleavage of ACE2 extracellular domain with a catalytic activity of Ang II degradation, and then the extracellular region was released into the extracellular environment. So, {beta}-chitosan could prevent the binding, internalization and degradation of ACE2 with SARS-CoV-2S-RBD and inhibit the activation of inflammatory signaling pathways at the same time. This work provides a valuable reference for the prevention and control of SARS-CoV-2 by {beta}-chitosan.
Full text:
Available
Collection:
Preprints
Database:
bioRxiv
Main subject:
Severe Acute Respiratory Syndrome
/
Inflammation
Language:
English
Year:
2020
Document Type:
Preprint
Similar
MEDLINE
...
LILACS
LIS