(-)-Epigallocatechin-3-gallate protects against uric acid-induced endothelial dysfunction in human umbilical vein endothelial cells

2019 ◽  
Vol 15 (63) ◽  
pp. 487
Author(s):  
Hua Xie ◽  
Jianqin Sun ◽  
Yanqiu Chen ◽  
Min Zong ◽  
Danfeng Xu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Uric Acid ◽  
Endothelial Dysfunction ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Anti-Inflammatory Properties of Sirtuin 6 in Human Umbilical Vein Endothelial Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Martha Lappas
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Histone Deacetylase ◽  
Proinflammatory Cytokines ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
Transcriptional Level ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

A prominent feature of inflammatory diseases is endothelial dysfunction. Factors associated with endothelial dysfunction include proinflammatory cytokines, adhesion molecules, and matrix degrading enzymes. At the transcriptional level, they are regulated by the histone deacetylase sirtuin (SIRT) 1 via its actions on the proinflammatory transcription factor nuclear factor-κB (NF-κB). The role of SIRT6, also a histone deacetylase, in regulating inflammation in endothelial cells is not known. The aim of this study was to determine the effect of SIRT6 knockdown on inflammatory markers in human umbilical vein endothelial cells (HUVECs) in the presence of lipopolysaccharide (LPS). LPS decreased expression of SIRT6 in HUVECs. Knockdown of SIRT6 increased the expression of proinflammatory cytokines (IL-1β, IL-6, IL-8), COX-prostaglandin system, ECM remodelling enzymes (MMP-2, MMP-9 and PAI-1), the adhesion molecule ICAM-1, and proangiogenic growth factors VEGF and FGF-2; cell migration; cell adhesion to leukocytes. Loss of SIRT6 increased the expression of NF-κB, whereas overexpression of SIRT6 was associated with decreased NF-κB transcriptional activity. Taken together, these results demonstrate that the loss of SIRT6 in endothelial cells is associated with upregulation of genes involved in inflammation, vascular remodelling, and angiogenesis. SIRT6 may be a potential pharmacological target for inflammatory vascular diseases.

Tetrahydrobiopterin correctsEscherichia coliendotoxin-induced endothelial dysfunction

2005 ◽  
Vol 289 (4) ◽  
pp. H1752-H1757 ◽  
Author(s):  
Friedrich Mittermayer ◽  
Johannes Pleiner ◽  
Georg Schaller ◽  
Stefan Zorn ◽  
Khodadad Namiranian ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Vitamin C ◽  
Acute Inflammation ◽  
Umbilical Vein ◽  
Oxidant Stress ◽  
Double Blind ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH4), the cofactor required for nitric oxide generation, is unclear. In this randomized, double-blind, three-way crossover study, forearm blood flow (FBF) responses to ACh and glyceryltrinitrate (GTN) were measured before and 3.5 h after infusion of Escherichia coli endotoxin (LPS, 20 IU/kg iv) in eight healthy men. The effect of intra-arterial BH4(500 μg/min), placebo, or vitamin C (24 mg/min) was studied on separate days 3.5 h after LPS infusion. In addition, human umbilical vein endothelial cells were incubated for 24 h with vitamin C and LPS. ACh and GTN caused dose-dependent forearm vasodilation. The FBF response to ACh, which was decreased by 23 ± 17% ( P < 0.05) by LPS infusion, was restored to baseline reactivity by BH4and vitamin C. FBF responses to GTN were not affected by BH4or vitamin C. LPS increased leukocyte count, high-sensitivity C-reactive protein, IL-6, IL-1β, IFN-γ, monocyte chemoattractant protein-1, pulse rate, and body temperature and decreased platelet count and vitamin C concentration. Vitamin C increased forearm plasma concentration of BH4by 32% ( P < 0.02). Incubation with LPS and vitamin C, but not LPS alone, increased intracellular BH4concentration in human umbilical vein endothelial cells. Impaired endothelial function during acute inflammation can be restored by BH4or vitamin C. Vitamin C may exert some of its salutary effects by increasing BH4concentration.

Low nanomolar caffeic acid attenuates high glucose-induced endothelial dysfunction in primary human umbilical-vein endothelial cells by affecting NF-κB and Nrf2 pathways

BioFactors ◽  
2016 ◽  
Vol 43 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Deborah Fratantonio ◽  
Antonio Speciale ◽  
Raffaella Canali ◽  
Lucia Natarelli ◽  
Daniela Ferrari ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Caffeic Acid ◽  
High Glucose ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Fang Wang ◽  
Linlin Zhao ◽  
Yingguang Shan ◽  
Ran Li ◽  
Guijun Qin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Cell Loss ◽  
Inflammatory Factors ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Aims. Inflammation was closely associated with diabetes-related endothelial dysfunction. C1q/tumor necrosis factor-related protein 3 (CTRP3) is a member of the CTRP family and can provide cardioprotection in many cardiovascular diseases via suppressing the production of inflammatory factors. However, the role of CTRP3 in high glucose- (HG-) related endothelial dysfunction remains unclear. This study evaluates the effects of CTRP3 on HG-induced cell inflammation and apoptosis. Materials and Methods. To prevent high glucose-induced cell injury, human umbilical vein endothelial cells (HUVECs) were pretreated with recombinant CTRP3 for 1 hour followed by normal glucose (5.5 mmol/l) or high glucose (33 mmol/l) treatment. After that, cell apoptosis and inflammatory factors were determined. Results. Our results demonstrated that CTRP3 mRNA and protein expression were significantly decreased after HG exposure in HUVECs. Recombinant human CTRP3 inhibited HG-induced accumulation of inflammatory factors and cell loss in HUVECs. CTRP3 treatment also increased the phosphorylation levels of protein kinase B (AKT/PKB) and the mammalian target of rapamycin (mTOR) in HUVECs. CTRP3 lost its inhibitory effects on HG-induced cell inflammation and apoptosis after AKT inhibition. Knockdown of endogenous CTRP3 in HUVECs resulted in increased inflammation and decreased cell viability in vitro. Conclusions. Taken together, these findings indicated that CTRP3 treatment blocked the accumulation of inflammatory factors and cell loss in HUVECs after HG exposure through the activation of AKT-mTOR signaling pathway. Thus, CTRP3 may be a potential therapeutic drug for the prevention of diabetes-related endothelial dysfunction.

Ginkgo biloba extract attenuates oxLDL-induced endothelial dysfunction via an AMPK-dependent mechanism

2013 ◽  
Vol 114 (2) ◽  
pp. 274-285 ◽  
Author(s):  
Hsiu-Chung Ou ◽  
Yueh-Ling Hsieh ◽  
Nae-Cherng Yang ◽  
Kun-Ling Tsai ◽  
Kai-Ling Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
Ginkgo Biloba ◽  
Umbilical Vein ◽  
Ginkgo Biloba Extract ◽  
No Synthase ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Dependent Mechanism

Atherosclerosis is a complex inflammatory arterial disease, and oxidized low-density lipoprotein (oxLDL) is directly associated with chronic vascular inflammation. Previous studies have shown that Ginkgo biloba extract (GbE) acts as a therapeutic agent for neurological and cardiovascular disorders. However, the mechanisms mediating the actions of GbE are still largely unknown. In the present study, we tested the hypothesis that GbE protects against oxLDL-induced endothelial dysfunction via an AMP-activated protein kinase (AMPK)-dependent mechanism. Human umbilical vein endothelial cells were treated with GbE, followed by oxLDL, for indicated time periods. Results from Western blot showed that GbE inhibited the membrane translocation of the NADPH oxidase subunits p47phox and Rac-1 and attenuated the increase in protein expression of membrane subunits gp91 and p22phox caused by oxLDL-induced AMPK dephosphorylation and subsequent PKC activation. AMPK-α1-specific small interfering RNA-transfected cells that had been exposed to GbE followed by oxLDL revealed elevated levels of PKC and p47phox. In addition, exposure to oxLDL resulted in reduced AMPK-mediated Akt/endothelial nitric oxide (NO) synthase signaling and the induction of phosphorylation of p38 mitogen-activated protein kinase, which, in turn, activated NF-κB-mediated inflammatory responses, such as the release of interleukin-8, the expression of the adhesion molecule, and the adherence of monocytic cells to human umbilical vein endothelial cells. Furthermore, oxLDL upregulated the expression of inducible NO synthase, thereby augmenting the formation of NO and protein nitrosylation. Pretreatment with GbE, however, exerted significant cytoprotective effects in a dose-dependent manner. Results from this study may provide insight into a possible molecular mechanism by which GbE protects against oxLDL-induced endothelial dysfunction.

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