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10.1016/j.prostaglandins.2021.106539

http://scihub22266oqcxt.onion/10.1016/j.prostaglandins.2021.106539
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33592322!7882227!33592322
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suck abstract from ncbi


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pmid33592322      Prostaglandins+Other+Lipid+Mediat 2021 ; 154 (ä): 106539
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  • Role of arachidonic cascade in COVID-19 infection: A review #MMPMID33592322
  • Ripon MAR; Bhowmik DR; Amin MT; Hossain MS
  • Prostaglandins Other Lipid Mediat 2021[Jun]; 154 (ä): 106539 PMID33592322show ga
  • The World Health Organization has described the 2019 Coronavirus disease caused by an influenza-like virus called SARS-CoV-2 as a pandemic. Millions of people worldwide are already infected by this virus, and severe infection causes hyper inflammation, thus disrupting lung function, exacerbating breath difficulties, and death. Various inflammatory mediators bio-synthesized through the arachidonic acid pathway play roles in developing cytokine storms, injuring virus-infected cells. Since pro-inflammatory eicosanoids, including prostaglandins, and leukotrienes, are key brokers for physiological processes such as inflammation, fever, allergy, and pain but, their function in COVID-19 is not well defined. This study addresses eicosanoid's crucial role through the arachidonic pathway in inflammatory cascading and recommends using bioactive lipids, NSAIDs, steroids, cell phospholipase A2 (cPLA2) inhibitors, and specialized pro-resolving mediators (SPMs) to treat COVID-19 disease. The role of soluble epoxide hydrolase inhibitors (SEHIs) in promoting the activity of epoxyeicosatrienoic acids (EETs) and 17-hydroxide-docosahexaenoic acid (17-HDHA) is also discussed. Additional research that assesses the eicosanoid profile in COVID-19 patients or preclinical models generates novel insights into coronavirus-host interaction and inflammation regulation.
  • |*COVID-19/epidemiology/metabolism[MESH]
  • |*Pandemics[MESH]
  • |Arachidonic Acids/*metabolism[MESH]
  • |Cytokine Release Syndrome/epidemiology/metabolism[MESH]
  • |Humans[MESH]
  • |Inflammation Mediators/*metabolism[MESH]


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