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.
What it is known about leukotriene receptor antagonists? •Leukotriene receptor antagonist, such as montelukast and zafirlukast, is used in asthma, COPD, and allergic rhinitis. • Montelukast is the most prescribed CysLT antagonist used in asthmatic patients. • Different in vivo animal studies have shown that leukotriene receptor antagonists can prevent the atherosclerosis progression, and have a protective role after cerebral ischemia. What we still need to know? • Today, there is a need for conducting clinical trials to assess the role of montelukast in reducing cardiovascular risk and to further understand the mechanism of action behind this effect.
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