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Protective role of N-acetylcysteine and Sulodexide on endothelial cells after SARS-CoV-2 infection (preprint)
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.07.19.549800
ABSTRACT

Objective:

Severe acute respiratory syndrome coronavirus-2 causes hyperinflammation and activation of coagulation cascade and in the result aggravates endothelial cell dysfunction. N-acetylcysteine and Sulodexide have been found to mitigate endothelial damage. Approach and

Results:

The influence on coronary artery endothelial cells of serum collected after 4+/-1 months from coronavirus infection was studied. The concentrations of serum samples of interleukin 6, von Willebrand Factor, tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 were studied. The cultures with serum of patients after coronavirus infection were incubated with N-acetylocysteine and Sulodexide to estimate their potential protective role. The blood inflammato-ry parameters were increased in the group of cultures incubated with serum from patients after coronavirus infection. Supplementation of the serum from patients after coronavirus infection with N-acetylcysteine or Sulodexide reduced the synthesis of interleukin 6, von Willebrand Fac-tor. No changes in the synthesis of tissue Plasminogen Activator were observed. N-acetylcysteine reduced the synthesis of Plasminogen Activator Inhibitor-1. N-acetylcysteine and Sulodexide increased the tPA/PAI-1 ratio.

Conclusion:

N-acetylcysteine may have a role in reducing the myocardial injury occurring in the post-COVID-19 syndrome. Sulodexide can also play a protective role in post-COVID-19 patients.
Subject(s)

Full text: Available Collection: Preprints Database: bioRxiv Main subject: Von Willebrand Diseases / Coronavirus Infections / COVID-19 / Cardiomyopathies Language: English Year: 2023 Document Type: Preprint

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Full text: Available Collection: Preprints Database: bioRxiv Main subject: Von Willebrand Diseases / Coronavirus Infections / COVID-19 / Cardiomyopathies Language: English Year: 2023 Document Type: Preprint