4.5 Article

Thymosin-α1 binds with ACE and downregulates the expression of ACE2 in human respiratory epithelia

期刊

FRONTIERS IN BIOSCIENCE-LANDMARK
卷 27, 期 2, 页码 -

出版社

IMR PRESS
DOI: 10.31083/j.fbl2702048

关键词

COVID-19; Thymosin-alpha 1; Angiotensin-converting enzyme 2 (ACE2); Angiotensin-converting enzyme (ACE)

资金

  1. National Key R&D Program of China [2020YFC2008304]
  2. National Natural Science Foundation of PR China [81973320, 81903714]
  3. Beijing Municipal Natural Science Foundation [7171012, 7204317]

向作者/读者索取更多资源

The study revealed that thymosin-alpha 1 prevents COVID-19 by binding with ACE and reducing ACE2 expression in human lung epithelial cells, suggesting its potential clinical applications in preventing SARS-CoV-2 infection.
Background: Thymosin-alpha 1 has been implicated into the treatment of novel respiratory virus Coronavirus Disease 2019 (COVID-19), but the underlying mechanisms are still disputable. Aim: Herein we aimed to reveal a previously unrecognized mechanism that thymosin-alpha 1 prevents COVID-19 by binding with angiotensin-converting enzyme (ACE), which was inspired from the tool of network pharmacology. Methods: KEG pathway enrichment of thymosin-alpha 1 treating COVID-19 was analyzed by Database of Functional Annotation Bioinformatics Microarray Analysis, then core targets were validated by ligand binding kinetics assay and fluorometric detection of ACE and ACE2 enzymatic activity. The production of angiotensin I, angiotensin II, angiotensin (1-7) and angiotensin (1-9) were detected by enzyme linked immunosorbent assay. Results: We found that thymosin-alpha 1 impaired the expressions of angiotensin-converting enzyme 2 and angiotensin (1-7) of human lung epithelial cells in a dose-dependent way (p < 0.001). In contrast, thymosin-alpha 1 had no impact on their ACE and angiotensin (1-9) expressions but significantly inhibited the enzymatic activity of ACE (p > 0.05). Conclusion: The bioinformatic findings of network pharmacology and the corresponding pharmacological validations have revealed that thymosin-alpha 1 treatment could decrease ACE2 expression in human lung epithelial cells, which strengthens the potential clinical applications of thymosin-alpha 1 to prevent severe acute respiratory syndrome coronavirus 2 infection.

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