scholarly journals An ethanol extract Gastrodia elata inhibits TNF‐α‐induced cell adhesion in human umbilical vein endothelial cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Sun Mi Hwang ◽  
Dae Gill Kang ◽  
Yun Jung Lee ◽  
Jin Sook Kim ◽  
Ho Sub Lee
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Ethanol Extract ◽  
Gastrodia Elata ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

Anti-Inflammatory Effect of Gastrodia elata Rhizome in Human Umbilical Vein Endothelial Cells

2009 ◽  
Vol 37 (02) ◽  
pp. 395-406 ◽  
Author(s):  
Sun Mi Hwang ◽  
Yun Jung Lee ◽  
Dae Gill Kang ◽  
Ho Sub Lee
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Gastrodia Elata ◽  
Human Umbilical Vein ◽  
Expression Levels ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Inflammatory Effect

Vascular inflammation is a pivotal factor of a variety of diseases, such as atherosclerosis and tumor progression. The present study was designed to examine the anti-inflammatory effect of ethanol extract of Gastrodia elata rhizome (EGE) in primary cultured human umbilical vein endothelial cells (HUVEC). Pretreatment of cells with EGE attenuated TNF-α-induced increase in expression levels of cell adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Real time qRT-PCR also showed that EGE decreased the mRNA expression levels of ICAM-1, VCAM-1, E-selectin as well as macrophage chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). In addition, EGE significantly inhibited TNF-α-induced increase in monocyte adhesion of HUVEC in a dose-dependent manner. Furthermore, EGE significantly inhibited TNF-α-induced intracellular reactive oxygen species (ROS) production and p65 NF-κB activation by preventing IκB-α phosphorylation. In conclusion, the present data suggest that EGE could suppress TNF-α-induced vascular inflammatory process via inhibition of oxidative stress and NF-κB activation in HUVEC.

Anti-Inflammatory Effect of Buddleja officinalis on Vascular Inflammation in Human Umbilical Vein Endothelial Cells

2010 ◽  
Vol 38 (03) ◽  
pp. 585-598 ◽  
Author(s):  
Yun Jung Lee ◽  
Mi Kyoung Moon ◽  
Sun Mi Hwang ◽  
Jung Joo Yoon ◽  
So Min Lee ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Vascular Inflammation ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Vascular inflammation process has been suggested to be an important risk factor in the initiation and development of atherosclerosis. In this study, we investigated whether and by what mechanisms an aqueous extract of Buddleja officinalis (ABO) inhibited the expressions of cellular adhesion molecules, which are relevant to inflammation and atherosclerosis. Pretreatment of human umbilical vein endothelial cells (HUVEC) with ABO (1–10 μg/ml) for 18 hours dose-dependently inhibited TNF-α-induced adhesion U937 monocytic cells, as well as mRNA and protein expressions of vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1). Pretreatment with ABO also blocked TNF-α-induced ROS formation. Nuclear factor-kappa B (NF-κB) is required in the transcription of these adhesion molecule genes. Western blot analysis revealed that ABO inhibits the translocation of the p65 subunit of NF-κB to the nucleus. ABO inhibited the TNF-α-induced degradation of IκB-α, an inhibitor of NF-κB, by inhibiting the phosphorylation of IκB-α in HUVEC. Taken together, ABO could reduce cytokine-induced endothelial adhesiveness throughout down-regulating intracellular ROS production, NF-κB, and adhesion molecule expression in HUVEC, suggesting that the natural herb Buddleja officinalis may have potential implications in atherosclerosis.

Febuxostat Attenuates the Induction of Vascular Cell Adhesion Protein 1 by TNF-α in Human Umbilical Vein Endothelial Cells

Pharmacology ◽  
2020 ◽  
pp. 1-7
Author(s):  
Yasuhiro Suzuki ◽  
Mari Deguchi ◽  
Airi Furuya ◽  
Sayuki Kato ◽  
Shoichiro Ohta
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Adhesion Protein ◽  
Human Umbilical Vein ◽  
Cell Adhesion Protein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

In a randomized trial, higher all-cause and cardiovascular mortality was observed in treatment with febuxostat than with allopurinol in patients with coexisting gout and serious cardiovascular conditions. In this study, we focus on an intervention of febuxostat or allopurinol as an anti-inflammatory treatment to reduce the transcription of nuclear factor-kappa B (NF-κB) and production of relevant inflammatory factors. We evaluated the effect of febuxostat on vascular cell adhesion protein 1 (VCAM-1) induction in cultured human umbilical vein endothelial cells (HUVECs). Cells were exposed to tumor necrosis factor (TNF)-α (10 ng/mL) treatment for 24 h. Febuxostat or allopurinol (0.1–100 μM) was added to the bath medium 15 min before TNF-α treatment. VCAM-1 levels in HUVECs increased after 24-h TNF-α treatment (<i>n</i> = 4). Febuxostat and allopurinol significantly suppressed VCAM-1 induced by treatment with TNF-α in a dose-dependent manner (<i>p</i> &#x3c; 0.05, <i>n</i> = 4). Furthermore, these drugs suppressed the NF-κB protein levels in the nucleus 4 h after TNF-α treatment (<i>n</i> = 3 or 4). Our results suggest that TNF-α induces VCAM-1 production via NF-κB, which can be blocked by febuxostat or allopurinol. The effect of febuxostat treatment on cardiovascular events may be associated with protection against the infiltration of lymphocytes or monocytes through VCAM-1 induction in inflamed endothelial cells such as arterial sclerosis.

Effects of recirculating flow on U-937 cell adhesion to human umbilical vein endothelial cells

1998 ◽  
Vol 275 (2) ◽  
pp. H591-H599 ◽  
Author(s):  
Kevin M. Barber ◽  
Aaron Pinero ◽  
George A. Truskey
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Fluid Velocity ◽  
Sudden Expansion ◽  
Reattachment Point ◽  
Human Umbilical Vein ◽  
Recirculating Flow ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

We used a sudden-expansion flow chamber to examine U-937 cell adhesion to unactivated and tumor necrosis factor (TNF)-α-activated human umbilical vein endothelial cells (HUVEC) in recirculating flow. For both unactivated and TNF-α-activated HUVEC, U-937 cells exhibited transient arrests within ∼150 μm of flow reattachment. Few arrests occurred directly at the reattachment site. U-937 cell rolling was not observed. At all other locations within the recirculation zone, U-937 cells did not exhibit transient arrests or rolling. TNF-α activation increased the frequency of U-937 cell arrests near reattachment but did not change the median arrest duration. Numerically simulated cell trajectories failed to predict attachment near the reattachment point. Deviations between experiment and theory may result from the nonspherical shape and deformability of U-937 cells. These results demonstrate that U-937 cell transient arrests occur preferentially in the vicinity of the reattachment point in recirculating flow. Possible mechanisms for adhesion include low shear stress, curved streamlines, fluid velocity components normal to the endothelium, and formation of larger contact areas.

Sinomenine suppresses TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells

2007 ◽  
Vol 114 (2) ◽  
pp. 180-185 ◽  
Author(s):  
Jianlin Huang ◽  
Zhuofeng Lin ◽  
Minqi Luo ◽  
Caisheng Lu ◽  
Michelle H. Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

scholarly journals Anti-Inflammatory and Anti-Apoptotic Effects of Stybenpropol A on Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 20 (21) ◽  
pp. 5383 ◽  
Author(s):  
Li Zhang ◽  
Feifei Wang ◽  
Qing Zhang ◽  
Qiuming Liang ◽  
Shumei Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Caspase 9 ◽  
Protein Levels ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Inflammation is a key mediator in the progression of atherosclerosis (AS). Benzoinum, a resin secreted from the bark of Styrax tonkinensis, has been widely used as a form of traditional Chinese medicine in clinical settings to enhance cardiovascular function, but the active components of the resin responsible for those pharmaceutical effects remain unclear. To better clarify these components, a new phenylpropane derivative termed stybenpropol A was isolated from benzoinum and characterized via comprehensive spectra a nalysis. We further assessed how this phenylpropane derivative affected treatment of human umbilical vein endothelial cells (HUVECs) with tumor necrosis factor-α (TNF-α). Our results revealed that stybenpropol A reduced soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-8 (IL-8), and interleukin-1β (IL-1β) expression by ELISA, inhibited apoptosis, and accelerated nitric oxide (NO) release in TNF-α-treated HUVECs. We further found that stybenpropol A decreased VCAM-1, ICAM-1, Bax, and caspase-9 protein levels, and increased the protein levels of Bcl-2, IKK-β, and IκB-α. This study identified a new, natural phenylpropane derivative of benzoinum, and is the first to reveal its cytoprotective effects in the context of TNF-α-treated HUVECs via regulation of the NF-κB and caspase-9 signaling pathways.

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