Table 2.
Possible role of Aspirin in COVID-19.
| Possible role of Aspirin in SARS-CoV-2 | Molecular mechanism of action | References |
|---|---|---|
| Anti-inflammatory effect | Non-selective inhibitor of cyclo-oxygenase (COX-1 and COX-2) enzymes | 34 |
| Inducing overactivation Heme oxygenase-1 | 35 | |
| Modulation of immune system and inhibition of viral replication and/or entry | Reducing reactive oxygen species (ROS) production and nuclear factor kappa beta (NF‐κB) activation | 7,26 |
| Stimulating over-expression of ubiquitin-protein ligase E6A, adenylosuccinate lyase, and nibrin | 25 | |
| Enhancing proteosomal degradation of claudin-1 | 36 | |
| Reducing virus affinity to CCAAT/enhancer-binding protein-beta (C/EBP-β) | 37 | |
| Enhancing the expression and activity of Cu/Zn superoxide dismutase (SOD1) | 38 | |
| Inhibiting of prostaglandin-E2 (PGE2) activity in macrophages and upregulating of interferon type I (IFN–I) production | 39 | |
| Dose dependent anti-viral activity with unknown molecular mechanism | 6 | |
| D-L lysine acetylsalicylate interferes NF- κB activation | 7 | |
| Anti-thrombotic effect | Inhibiting the production of Thromboxane-A2 | 22, 34, |
| Acetylation of proteins (e.g., fibrinogen) involved in the coagulation cascade | 33 |