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10.1016/j.biopha.2021.111437 http://scihub22266oqcxt.onion/10.1016/j.biopha.2021.111437 33691249!7904450!33691249     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biomed+Pharmacother 2021 ; 138 (ä): 111437 Nephropedia Template TP {{tp|p=33691249|t=2021. Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection |pdf=|usr=}}{{33691249}} gab.com Text Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection JO: Biomed Pharmacother http://www.kidney.de/pget.php?&tw=1&pmid=33691249 #FOAvip Hyperinflammatory response caused by infections such as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) increases organ failure, intensive care unit admission, and mortality. Cytokine storm in patients with Coronavirus Disease 2019 (COVID-19) drives this pattern of poor clinical outcomes and is dependent upon the activity of the transcription factor complex nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) and its downstream target gene interleukin 6 (IL6) which interacts with IL6 receptor (IL6R) and the IL6 signal transduction protein (IL6ST or gp130) to regulate intracellular inflammatory pathways. In this study, we compare transcriptomic signatures from a variety of drug-treated or genetically suppressed (i.e. knockdown) cell lines in order to identify a mechanism by which antidepressants such as fluoxetine demonstrate non-serotonergic, anti-inflammatory effects. Our results demonstrate a critical role for IL6ST and NF-kappaB Subunit 1 (NFKB1) in fluoxetine's ability to act as a potential therapy for hyperinflammatory states such as asthma, sepsis, and COVID-19. Twit Text FOAVip Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection ????Biomed Pharmacother http://www.kidney.de/pget.php?&tw=1&pmid=33691249 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33691249 #FOAvip English Wikipedia <ref>{{Cite pmid|33691249}}</ref> Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection #MMPMID33691249 Creeden JF; Imami AS; Eby HM; Gillman C; Becker KN; Reigle J; Andari E; Pan ZK; O'Donovan SM; McCullumsmith RE; McCullumsmith CB Biomed Pharmacother 2021[Jun]; 138 (ä): 111437 PMID33691249show ga Hyperinflammatory response caused by infections such as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) increases organ failure, intensive care unit admission, and mortality. Cytokine storm in patients with Coronavirus Disease 2019 (COVID-19) drives this pattern of poor clinical outcomes and is dependent upon the activity of the transcription factor complex nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) and its downstream target gene interleukin 6 (IL6) which interacts with IL6 receptor (IL6R) and the IL6 signal transduction protein (IL6ST or gp130) to regulate intracellular inflammatory pathways. In this study, we compare transcriptomic signatures from a variety of drug-treated or genetically suppressed (i.e. knockdown) cell lines in order to identify a mechanism by which antidepressants such as fluoxetine demonstrate non-serotonergic, anti-inflammatory effects. Our results demonstrate a critical role for IL6ST and NF-kappaB Subunit 1 (NFKB1) in fluoxetine's ability to act as a potential therapy for hyperinflammatory states such as asthma, sepsis, and COVID-19. |*COVID-19 Drug Treatment[MESH] |*SARS-CoV-2[MESH] |Anti-Inflammatory Agents/pharmacology/*therapeutic use[MESH] |Cytokine Receptor gp130/*genetics[MESH] |Cytokine Release Syndrome/*drug therapy[MESH] |Fluoxetine/pharmacology/*therapeutic use[MESH] |Humans[MESH]Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection (epmc).pdf DeepDyve Pubget Overpricing