Fig. 1.

HCQ exhibits antioxidant and anti-inflammatory effects. SARS-CoV causes the phosphorylation and activation of p38 mitogen-activated protein kinase (p38). Then activated p38 causes the activation of classical heterodimeric (p65:p50) NF-κB, a proinflammatory transcription factor. Together with activated p300 (a proinflammatory histone acetyl transferase), the NF-κB then binds to the promoter of different genes ultimately leading to the transcription and production of different proinflammatory molecules (e.g. tumor necrosis factor alpha or TNFα, interleukin-1β or IL-1β, etc.). HCQ inhibits the phosphorylation of p38 to attenuate the production of different proinflammatory cytokines. Again, activation of NADPH oxidase (a pentameric complex of gp91phox, p67phox, p47phox, p22phox, and Rac) produces superoxide radicals to cause oxidative stress and the activation of NF-κB for inflammation. HCQ prevents the translocation of gp91phox to the membrane and thereby inhibits the activation of NADPH oxidase to reduce oxidative stress and inflammation