PMC:7781431 / 34445-36506 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7781431","sourcedb":"PMC","sourceid":"7781431","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7781431","text":"SARS-CoV-2\nSevere acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) refers to a coronavirus strain that causes 2019 coronavirus disease (COVID-19), a respiratory disease that is the cause of the COVID-19 pandemic (Coronaviridae Study Group of the International Committee on Taxonomy of, 2020). SARS-CoV-2 is an RNA virus that infects the lungs and causes deaths through complications such as cytokine storms (Goldin et al. 2020).\nThe anti-inflammatory action of mesenchymal stem cells is well known, and it is believed that these mesenchymal stem cells exhibit anti-inflammatory action through PGE2 and LXA4. These lipids mediators alleviate the SARS-CoV-2 cytokine storm, while arachidonic acid, dihomo-gamma-linolenic acid, and gamma-linolenic acid inactivate enveloped viruses (Das 2020). Obesity is a risk factor for SARS-CoV-2 infection, and a BMI of 30 kg/m2 increases the risk of infection by 61% (Bello-Chavolla et al. 2020). This is likely due to a deficiency of SPMs in obese patients, and this deficiency promotes adverse reactions during SARS-CoV-2 infection (Pal et al. 2020). LXA4, Elovanoid-N32 or RvD6 isomers reduced expression of angiotensin-converting enzyme 2 (ACE2), but NDP1 did not reduce it. These lipids mediators also counteract the binding of the receptor-binding domain (RBD) of SARS-CoV-2 spike (S) protein to the injured cornea (Figs. 3 and 4) (Pham et al. 2020). Elovanoid-N32 or RvD6 isomers also attenuated the expression of cytokines involved in a cytokine storm and hyperinflammation. Based on previous study results that have demonstrated SPMs as potential therapeutic targets for SARS-CoV-2 infection, studies and review on the use of fish oil, an SPMs precursor, as an adjuvant are in progress. (Torrinhas et al. 2020; Rogero et al. 2020). SPMs and soluble epoxide hydrolase inhibitors are currently in clinical trials for other inflammatory diseases and can be quickly converted and used for SARS-CoV-2 management through the removal of cellular debris and inhibition of inflammatory cytokines (Panigrahy et al. 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