Alamandine: Potential Protective Effects in SARS-CoV-2 Patients

Figure 2

Proposed mechanisms by which alamandine inhibits the SARS-CoV-2-related cytokine storm and accompanying damage. The binding of SARS-CoV-2 to the ACE2 receptor may increase ROS production by epithelial cells. ROS, in turn, may cause cell death and increase the synthesis of NF-κB and NLRP3, both of which increase cytokine levels. This phenomenon leads to immunological infiltration, which may cause illnesses such as acute respiratory distress syndrome, sepsis, and, in severe instances, death. Alamandine may mitigate these effects by increasing the levels of antioxidant enzymes (SOD, GPx) and decreasing the levels of proinflammatory cytokines (IL-1β and IL-6), proinflammatory transcription factor (NF-κB), the profibrotic mediator (TGF-β), and the apoptotic factor (caspase 3). ACE2: angiotensin-converting enzyme-2; MrgD: Mas-related G protein-coupled receptor D; ROS: reactive oxygen species; NLRP3: NOD-, LRR-, and pyrin domain-containing protein 3; NF-κB: nuclear factor kappa beta; IL: interleukin; SOD: superoxide dismutase; GPx: glutathione peroxidase; TGF-β: transforming growth factor-β; TNF-α: tumor necrosis factor α; IFN-γ: interferon-gamma.