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10.18632/aging.202692 http://scihub22266oqcxt.onion/10.18632/aging.202692 33839697!8064163!33839697     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33839697&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33839697.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Aging+(Albany+NY) 2021 ; 13 (7): 9582-9591 Nephropedia Template TP {{tp|p=33839697|t=2021. LCZ696 ameliorates lipopolysaccharide-induced endothelial injury |pdf=|usr=}}{{33839697}} gab.com Text LCZ696 ameliorates lipopolysaccharide-induced endothelial injury JO: Aging (Albany NY) http://www.kidney.de/pget.php?&tw=1&pmid=33839697 #FOAvip Lipopolysaccharide (LPS)-induced endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases. LCZ696, the dual-acting angiotensin receptor blocker, and neprilysin inhibitor has been used for the treatment of heart failure with reduced ejection fraction. Recent work suggests that LCZ696 therapy might have an anti-inflammatory effect in cardiovascular tissue. In the current study, we show that LCZ696 attenuates LPS-induced oxidative stress by reducing the production of intracellular reactive oxygen species (ROS) and the measurements of malonyl dialdehyde (MDA) level in human umbilical vascular endothelial cells (HUVECs). LCZ696 inhibits LPS-induced expressions and secretions of the pro-inflammatory cytokines, interleukin-6 (IL-6), interleukin-1alpha (IL-1alpha), and tumor necrosis factor beta (TNF-beta) as well as the chemokines, monocyte chemotactic protein 1 (MCP-1), and chemokine (C-X-C motif) ligand 1 protein (CXCL1). Additionally, we found that LCZ696 reduces LPS-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and P-selectin and the attachment of U937 monocytes to HUVECs. Mechanistically, LCZ696 prevents LPS-induced activation of the TLR4/Myd88 pathway and nuclear translocation of nuclear factor kappa-B (NF-kappaB) p65 factor. Based on these findings, we conclude that LCZ696 is capable of ameliorating LPS-induced endothelial dysfunction via anti-inflammatory properties. Twit Text FOAVip LCZ696 ameliorates lipopolysaccharide-induced endothelial injury ????Aging (Albany NY) http://www.kidney.de/pget.php?&tw=1&pmid=33839697 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33839697 #FOAvip English Wikipedia <ref>{{Cite pmid|33839697}}</ref> LCZ696 ameliorates lipopolysaccharide-induced endothelial injury #MMPMID33839697 Gao A; Wang Y; Gao X; Tian W Aging (Albany NY) 2021[Apr]; 13 (7): 9582-9591 PMID33839697show ga Lipopolysaccharide (LPS)-induced endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases. LCZ696, the dual-acting angiotensin receptor blocker, and neprilysin inhibitor has been used for the treatment of heart failure with reduced ejection fraction. Recent work suggests that LCZ696 therapy might have an anti-inflammatory effect in cardiovascular tissue. In the current study, we show that LCZ696 attenuates LPS-induced oxidative stress by reducing the production of intracellular reactive oxygen species (ROS) and the measurements of malonyl dialdehyde (MDA) level in human umbilical vascular endothelial cells (HUVECs). LCZ696 inhibits LPS-induced expressions and secretions of the pro-inflammatory cytokines, interleukin-6 (IL-6), interleukin-1alpha (IL-1alpha), and tumor necrosis factor beta (TNF-beta) as well as the chemokines, monocyte chemotactic protein 1 (MCP-1), and chemokine (C-X-C motif) ligand 1 protein (CXCL1). Additionally, we found that LCZ696 reduces LPS-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and P-selectin and the attachment of U937 monocytes to HUVECs. Mechanistically, LCZ696 prevents LPS-induced activation of the TLR4/Myd88 pathway and nuclear translocation of nuclear factor kappa-B (NF-kappaB) p65 factor. Based on these findings, we conclude that LCZ696 is capable of ameliorating LPS-induced endothelial dysfunction via anti-inflammatory properties. |Aminobutyrates/*pharmacology[MESH] |Biphenyl Compounds/*pharmacology[MESH] |Cytokines/metabolism[MESH] |Drug Combinations[MESH] |Human Umbilical Vein Endothelial Cells/*drug effects/metabolism[MESH] |Humans[MESH] |Lipopolysaccharides/pharmacology[MESH] |Malondialdehyde/metabolism[MESH] |Oxidative Stress/*drug effects[MESH] |Protective Agents/*pharmacology[MESH] |Reactive Oxygen Species/*metabolism[MESH] |Signal Transduction/drug effects[MESH] |Valsartan/*pharmacology[MESH]LCZ696 ameliorates lipopolysaccharide-induced endothelial injury (epmc).pdf DeepDyve Pubget Overpricing