Magnesium sulfate suppresses inflammatory responses by human umbilical vein endothelial cells (HuVECs) through the NFκB pathway

2007 ◽  
Vol 73 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Burton Rochelson ◽  
Oonagh Dowling ◽  
Nadav Schwartz ◽  
Christine N. Metz
Keyword(s):  
Endothelial Cells ◽  
Magnesium Sulfate ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Nfκb Pathway ◽  
Umbilical Vein Endothelial Cells

scholarly journals Magnesium sulfate inhibits inflammation through P2X7 receptors in human umbilical vein endothelial cells

2019 ◽  
Vol 87 (3) ◽  
pp. 463-471 ◽  
Author(s):  
Maide Ozen ◽  
Han Xie ◽  
Na Shin ◽  
Ghada Al Yousif ◽  
Julia Clemens ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Magnesium Sulfate ◽  
Umbilical Vein ◽  
P2x7 Receptors ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Factor Xa inhibits HMGB1-induced septic responses in human umbilical vein endothelial cells and in mice

2014 ◽  
Vol 112 (10) ◽  
pp. 757-769 ◽  
Author(s):  
Wonhwa Lee ◽  
Sae-Kwang Ku ◽  
Jong-Sup Bae
Keyword(s):  
Endothelial Cells ◽  
Nuclear Dna ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Cecal Ligation ◽  
Post Treatment ◽  
Coagulation Cascade ◽  
Factor X ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

SummaryNuclear DNA-binding protein high mobility group box 1 (HMGB1) acts as a late mediator of severe vascular inflammatory conditions, such as sepsis. Activated factor X (FXa) is an important player in the coagulation cascade responsible for thrombin generation, and it influences cell signalling in various cell types by activating protease-activated receptors (PARs). However, the effect of FXa on HMGB1-induced inflammatory response has not been studied. First, we addressed this issue by monitoring the effects of post-treatment with FXa on lipopolysaccharide (LPS)- and cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated regulation of pro-inflammatory responses in human umbilical vein endothelial cells (HUVECs) and septic mice. Post-treatment with FXa was found to suppress LPS-mediated release of HMGB1 and HMGB1-mediated cytoskeletal rearrangements. FXa also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in septic mice. In addition, FXa inhibited the production of tumour necrosis factor-α and interleukin (IL)-1β. FXa also facilitated the downregulation of CLP-induced release of HMGB1, production of IL-6, and mortality. Collectively, these results suggest that FXa may be regarded as a candidate therapeutic agent for treating vascular inflammatory diseases by inhibiting the HMGB1 signalling pathway.

scholarly journals Evodiamine Attenuates P2X7-Mediated Inflammatory Injury of Human Umbilical Vein Endothelial Cells Exposed to High Free Fatty Acids

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yun Xue ◽  
Ting Guo ◽  
Lifang Zou ◽  
Yingxin Gong ◽  
Bing Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Endothelial Cells ◽  
Free Fatty Acids ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Insulin resistance and type 2 diabetes mellitus (T2DM) are highly prevalent around the world. Elevated concentrations of free fatty acids (FFAs) are closely related to insulin resistance and T2DM. P2X7 receptor is an ion channel gated by ATP, which is implicated in various scenarios including immune response, pain, and inflammation. In this study, we have explored whether P2X7 receptor is involved in pathological changes in human umbilical vein endothelial cells (HUVECs) induced by high FFA treatment, and the potential beneficial effects of evodiamine. Evodiamine could effectively suppress the enhanced expression of P2X7 receptor caused by high FFAs at both mRNA and protein levels. In addition, high FFA-induced cytotoxicity, the upregulated release of ATP, and production of reactive oxygen species (ROS) could be ameliorated by evodiamine in HUVECs. Evodiamine could also reverse the decreased NO formation and the increased adhesive events of immune cells at high FFAs. Moreover, evodiamine inhibited P2X7-dependent TNF-α expression and ERK 1/2 phosphorylation due to high FFAs. All these results indicated that evodiamine could correct the upregulated expression of P2X7 receptor induced under high FFA condition in HUVECs, and consequently suppressed oxidative stress and inflammatory responses.

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