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10.1038/s41598-021-91794-z

http://scihub22266oqcxt.onion/10.1038/s41598-021-91794-z
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suck abstract from ncbi


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pmid34112906      Sci+Rep 2021 ; 11 (1): 12324
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  • Elovanoids downregulate SARS-CoV-2 cell-entry, canonical mediators and enhance protective signaling in human alveolar cells #MMPMID34112906
  • Calandria JM; Bhattacharjee S; Maness NJ; Kautzmann MI; Asatryan A; Gordon WC; Do KV; Jun B; Mukherjee PK; Petasis NA; Bazan NG
  • Sci Rep 2021[Jun]; 11 (1): 12324 PMID34112906show ga
  • The pro-homeostatic lipid mediators elovanoids (ELVs) attenuate cell binding and entrance of the SARS-CoV-2 receptor-binding domain (RBD) as well as of the SARS-CoV-2 virus in human primary alveoli cells in culture. We uncovered that very-long-chain polyunsaturated fatty acid precursors (VLC-PUFA, n-3) activate ELV biosynthesis in lung cells. Both ELVs and their precursors reduce the binding to RBD. ELVs downregulate angiotensin-converting enzyme 2 (ACE2) and enhance the expression of a set of protective proteins hindering cell surface virus binding and upregulating defensive proteins against lung damage. In addition, ELVs and their precursors decreased the signal of spike (S) protein found in SARS-CoV-2 infected cells, suggesting that the lipids curb viral infection. These findings open avenues for potential preventive and disease-modifiable therapeutic approaches for COVID-19.
  • |*COVID-19 Drug Treatment[MESH]
  • |Alveolar Epithelial Cells/drug effects/metabolism[MESH]
  • |Angiotensin-Converting Enzyme 2/metabolism[MESH]
  • |Antiviral Agents/chemistry/*pharmacology[MESH]
  • |COVID-19/metabolism[MESH]
  • |Cells, Cultured[MESH]
  • |Humans[MESH]
  • |SARS-CoV-2/*drug effects/physiology[MESH]
  • |Signal Transduction/*drug effects[MESH]
  • |Spike Glycoprotein, Coronavirus/metabolism[MESH]


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