Chloroquine inhibits stimulated platelets at the arachidonic acid pathway
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Can hydroxychloroquine be protective against COVID-19-associated thrombotic events ?
2021, Journal of Microbiology, Immunology and InfectionCitation Excerpt :The antithrombotic properties of HCQ was described as far as 1975.5 In the context of autoimmune disease (SLE), HCQ inhibits stimulated platelets at the arachidonic acid pathway and thromboxane 2 generation in activated platelets (an activator of platelets aggregation), which is associated with decreased circulating levels of endothelin-1, and allows improvement of endothelial function.3,6–8 Interestingly, using network-based approach to prediction and population-based validation of in silico drug repurposing it was found that the Healthcare registry data for 220 million people showed that HCQ intake (a series of 37,795 patients receiving HCQ) was associated with a lower risk for coronary artery disease.9
COVID-19: Immunology and treatment options
2020, Clinical ImmunologyCitation Excerpt :Furthermore, preventing the acidification of lysosomes, hydroxychloroquine impairs cellular autophagy, a critical step for innate and adaptive immunity activation [132]. Finally, hydroxychloroquine has antithrombotic effects, which may be beneficial in COVID-19, where inflammatory stimuli and endothelial injury activate coagulation and promote micro-thrombus formation [133,134]. While generally deemed safe when administered at correct dosing and under close monitoring, the therapeutic range of chloroquine and its derivatives is narrow.
Effects of 5,8-dimethylthieno[2,3-b]quinoline-2-carboxylic acid on the antioxidative defense and lipid membranes in Plasmodium berghei-infected erythrocytes
2015, Experimental ParasitologyCitation Excerpt :In this context, Jackson et al. (1984) demonstrated the ability of chloroquine to induce oxidative stress and to inhibit lipid peroxidation, possibly as a phospholipase-A2 inhibitor. Indeed, it was reported that this compound inhibited arachidonic acid liberation from membrane phospholipids (Nosál et al., 1995), thus, due to the same quinolone basic structure, TQCA could also inhibit lipid peroxidation by this mechanism. Further studies are needed to confirm this hypothesis.
Hydroxychloroquine as an anti-thrombotic in antiphospholipid syndrome
2015, Autoimmunity ReviewsCitation Excerpt :In a dose-dependent fashion, HCQ and CQ can reduce collagen-induced platelet aggregation and platelet alpha-granule release [24,25]. HCQ can also reduce ADP-induced and/or ristocetin platelet aggregation [23,24], as well as arachidonic acid release by activated platelets [26]. This effect seems to be related to the inhibition of phospholipase A2 activation.
Antimalarials in dermatology: Mechanism of action, Indications, and side effects
2014, Actas Dermo-Sifiliograficas