Table 2.
Effect | Mechanism of action |
---|---|
Anti-infectious | Antimicrobial effects on HIV, coronavirus, influenza viruses. |
Anti-inflammatory effects | Inhibition of phospholipase A2 and C. Inhibition of formation of IL1β, TNF-α. Inhibition of mast cells. Inhibition of Toll-like receptor 9 signal pathway. |
Antiproliferative | Inhibits protein synthesis Promote chemo sensitization. Inhibit cell growth or cell death or both. Prevent mutations in cells with high mitotic rates. |
Effect on coagulation | Inhibit platelet aggregation and adhesion. Inhibit formation of antiphospholipid antibody-β2-glycoprotein 1 complexes. Prevent antiphospholipid antibody binding of annexin-5 |
Immunological | Inhibits autoantigen processing (MHCII). |
Response | Reduced stimulation of autoreactive CD4+ T cells Reduced cytokine production: Reduces serum interleukin (IL)-1β, IL-6, IL-18, and tumor necrosis factor-alpha (TNF-α)(takes 3 months)[10] IL-18, is the interferon gamma (IFN-γ)-inducing factor, thus its reduction affects the adaptive immunity.[11] CQ inhibits macrophage TNF- α mRNA transcription and endotoxin induced secretion of TNF- α, IL-1, and IL-6. Binding to DNA and thus competitive inhibition of anti-DNA antibodies. Block of activation of innate and adaptive immunity process mediated by Toll-like receptors.[12] |
Metabolic | Decreased hydroxylation of Vitamin D Lowered levels of LDL, Triglycerides and cholesterol. Increased excretion of porphyrin due to complex formation of HCQ with porphyrin |
Photoprotective | Increased UV filtration? (Questionable relevance). It can cause spectral shift due to accumulation in melanin and increase in epidermal concentrations Inhibition of UV-induced inflammatory reactions |