Abstract
The coronavirus disease 2019 (COVID-19) pandemic is caused by a novel severe acute respiratory syndrome (SARS)-like coronavirus (SARS-CoV-2). Here, we review the molecular pathogenesis of SARS-CoV-2 and its relationship with oxidative stress (OS) and inflammation. Furthermore, we analyze the potential role of antioxidant and anti-inflammatory therapies to prevent severe complications. OS has a potential key role in the COVID-19 pathogenesis by triggering the NOD-like receptor family pyrin domain containing 3 inflammasome and nuclear factor-kB (NF-kB). While exposure to many pro-oxidants usually induces nuclear factor erythroid 2 p45-related factor2 (NRF2) activation and upregulation of antioxidant related elements expression, respiratory viral infections often inhibit NRF2 and/or activate NF-kB pathways, resulting in inflammation and oxidative injury. Hence, the use of radical scavengers like N-acetylcysteine and vitamin C, as well as of steroids and inflammasome inhibitors, has been proposed. The NRF2 pathway has been shown to be suppressed in severe SARS-CoV-2 patients. Pharmacological NRF2 inducers have been reported to inhibit SARS-CoV-2 replication, the inflammatory response, and transmembrane protease serine 2 activation, which for the entry of SARS-CoV-2 into the host cells through the angiotensin converting enzyme 2 receptor. Thus, NRF2 activation may represent a potential path out of the woods in COVID-19 pandemic.
Highlights
severe acute respiratory syndrome (SARS)-CoV-2 is dissimilar from the coronaviruses recognized to induce the ordinary cold, but it has been shown to have the same characteristics as the zoonotic SARS coronavirus (SARS-CoV) [4] and the Middle East respiratory syndrome (MERS) coronavirus [5]
One crucial discovery in learning how SARS-CoV-2 enters into the cells involves the role of transmembrane protease serine 2 (TMPRSS2), a cell-surface protein [56] (Figure 2) that was identified in 2001 in the role of TMPRSS2, a cell-surface protein [56] (Figure 2) that was identified in 2001 in the epithelia of the gastrointestinal, urogenital, and respiratory tracts of mouse and humans, epithelia of the gastrointestinal, urogenital, and respiratory tracts of mouse and humans, TMPRSS2 expression in human dominates in the prostate [57]
Every 8 h for 3 days reported decreased mortality, decreased intubation and mechanical ventilation need and a significant decrease in inflammatory markers, including ferritin and D-dimer, and a trend towards decreasing FiO2 requirements [172]. These parameters are under investigation in the “Intravenous Vitamin C Administration in Coronavirus (COVID-19) and Decreased Oxygenation (AVoCaDO), NCT04357782” clinical trial in which subjects administered with intravenous Vitamin C are supposed to be at lower risk of respiratory failure worsening and reduced inflammation markers increase
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Patients affected by COVID-19 often display no symptoms or mild symptoms (fever, cough, myalgia, and fatigue) and usually have a good prognosis. Many of these cases, progress to a more severe form of the illness, especially in older men experiencing other contemporary serious diseases [2,6,7,8]. ACE2 was recognized as the functional receptor for SARS-CoV after the fusion protein gene of SARS-CoV was Antioxidants 2021, 10, 272. Studies in vivo have clearly shown that ACE2 is a pivotal SARS-CoV receptor [28]. We analyze the potential role of antioxidant and antiinflammatory therapies to prevent severe complications
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