4.3 Article

What about COVID-19 and arachidonic acid pathway?

Journal

EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY
Volume 76, Issue 11, Pages 1501-1504

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00228-020-02941-w

Keywords

Arachidonic acid; COVID-19; Prostaglandins; Leukotrienes; Eicosanoids; Thromboxane

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Background and objective COVID-19 is a highly contagious viral disease. In this study, we tried to define and discuss all the findings on the potential association between arachidonic acid (AA) pathway and COVID-19 pathophysiology. Methods A literature search across PubMed, Scopus, Embase, and Cochrane database was conducted. A total of 25 studies were identified. Results The data elucidated that COX-2 and prostaglandins (PGs), particularly PGE(2), have pro-inflammatory action in COVID-19 pathophysiology. Arachidonic acid can act as endogenous antiviral compound. A deficiency in AA can make humans more susceptible to COVID-19. Targeting these pro-inflammatory mediators may help in decreasing the mortality and morbidity rate in COVID-19 patients. Conclusions PGE(2)levels and other PGs levels should be measured in patients with COVID-19. Lowering the PGE(2)levels through inhibition of human microsomal prostaglandin E synthase-1 (mPGES-1) can enhance the host immune response against COVID-19. In addition, the hybrid compounds, such as COX-2 inhibitors/TP antagonists, can be an innovative treatment to control the overall balance between AA mediators in patients with COVID-19.

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