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10.1016/j.jri.2006.06.004 http://scihub22266oqcxt.onion/10.1016/j.jri.2006.06.004 16952401!ä!16952401 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=16952401&cmd=llinks): Failed to open stream: HTTP request failed! 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Magnesium sulfate suppresses inflammatory responses by human umbilical vein endothelial cells (HuVECs) through the NFkappaB pathway |pdf=|usr=}}{{16952401}} gab.com Text Magnesium sulfate suppresses inflammatory responses by human umbilical vein endothelial cells (HuVECs) through the NFkappaB pathway JO: J Reprod Immunol http://www.kidney.de/pget.php?&tw=1&pmid=16952401 #FOAvip Dysfunctional endothelial cell activation and cytokines are implicated in preterm labor, a condition commonly treated with the tocolytic agent, magnesium sulfate (MgSO(4)). Based on recent findings showing the inflammatory effects of magnesium deficiency, we examined the effect of MgSO(4) on human umbilical vein endothelial cell (HuVEC) inflammatory responses in vitro. HuVECs isolated from term umbilical cords were incubated with MgSO(4) prior to stimulation with lipopolysaccharide (LPS) and then assessed for endothelial cell activation. Endothelial cell supernatants were assayed for inflammatory mediator production (interleukin-8; IL-8), and endothelial cell-associated intercellular adhesion molecule (ICAM-1) expression was determined. In the absence of LPS stimulation, MgSO(4) had no effect on HuVEC responses. Treatment of HuVECs with MgSO(4) prior to LPS stimulation inhibited inflammatory mediator production (p<0.05) and cell adhesion molecule expression (p<0.05) in a dose-dependent manner. Mechanistic studies showed that MgSO(4) reduced NFkappaB nuclear translocation and protected cytoplasmic IkappaBalpha from degradation in LPS-treated HuVECs. In conclusion, MgSO(4) inhibits endothelial cell activation, as measured by levels of IL-8 and ICAM-1 expression, via NFkappaB. Our results support the hypothesis that MgSO(4) treatment may function as an anti-inflammatory agent during preterm labor. Twit Text FOAVip Magnesium sulfate suppresses inflammatory responses by human umbilical vein endothelial cells (HuVECs) through the NFkappaB pathway ????J Reprod Immunol http://www.kidney.de/pget.php?&tw=1&pmid=16952401 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=16952401 #FOAvip English Wikipedia <ref>{{Cite pmid|16952401}}</ref> Magnesium sulfate suppresses inflammatory responses by human umbilical vein endothelial cells (HuVECs) through the NFkappaB pathway #MMPMID16952401 Rochelson B; Dowling O; Schwartz N; Metz CN J Reprod Immunol 2007[Apr]; 73 (2): 101-107 PMID16952401show ga Dysfunctional endothelial cell activation and cytokines are implicated in preterm labor, a condition commonly treated with the tocolytic agent, magnesium sulfate (MgSO(4)). Based on recent findings showing the inflammatory effects of magnesium deficiency, we examined the effect of MgSO(4) on human umbilical vein endothelial cell (HuVEC) inflammatory responses in vitro. HuVECs isolated from term umbilical cords were incubated with MgSO(4) prior to stimulation with lipopolysaccharide (LPS) and then assessed for endothelial cell activation. Endothelial cell supernatants were assayed for inflammatory mediator production (interleukin-8; IL-8), and endothelial cell-associated intercellular adhesion molecule (ICAM-1) expression was determined. In the absence of LPS stimulation, MgSO(4) had no effect on HuVEC responses. Treatment of HuVECs with MgSO(4) prior to LPS stimulation inhibited inflammatory mediator production (p<0.05) and cell adhesion molecule expression (p<0.05) in a dose-dependent manner. Mechanistic studies showed that MgSO(4) reduced NFkappaB nuclear translocation and protected cytoplasmic IkappaBalpha from degradation in LPS-treated HuVECs. In conclusion, MgSO(4) inhibits endothelial cell activation, as measured by levels of IL-8 and ICAM-1 expression, via NFkappaB. Our results support the hypothesis that MgSO(4) treatment may function as an anti-inflammatory agent during preterm labor. |Active Transport, Cell Nucleus/drug effects/immunology[MESH] |Cell Adhesion/drug effects/immunology[MESH] |Cell Nucleus/immunology[MESH] |Cells, Cultured[MESH] |Endothelial Cells/*immunology/pathology[MESH] |Female[MESH] |Humans[MESH] |I-kappa B Proteins/immunology[MESH] |Inflammation Mediators/immunology[MESH] |Inflammation/immunology/pathology[MESH] |Intercellular Adhesion Molecule-1/immunology[MESH] |Interleukin-8/*immunology[MESH] |Lipopolysaccharides/pharmacology[MESH] |Magnesium Sulfate/*pharmacology[MESH] |NF-KappaB Inhibitor alpha[MESH] |NF-kappa B/*immunology[MESH] |Pregnancy[MESH] |Premature Birth/immunology/pathology[MESH] |Tocolytic Agents/*pharmacology[MESH]Magnesium sulfate suppresses inflammatory responses by human umbilical(epmc).pdf DeepDyve Pubget Overpricing