Serum biomarkers of ED (sVCAM-1, E-selectin, P-selectin, thrombomodulin, sICAM-1, sICAM-3) and LGI (hs-CRP, SAA, IL-6, IL-8, TNF-α) were measured with a single- or multiplex array detection system based on electro-chemiluminescence technology.
Impressic Acid, a Lupane-Type Triterpenoid from <i>Acanthopanax koreanum</i>, Attenuates TNF-α-Induced Endothelial Dysfunction via Activation of eNOS/NO Pathway.
The HIV-1-proteins Tat, Gp120 and Nef in particular, the proinflammatory cytokine, TNF-α, and the antiretroviral drugs Efavirenz and Lopinavir, most commonly postulated to be primary causal agents of endothelial dysfunction, are also discussed.
Pro-inflammatory T cell-derived cytokines such as IFN-γ and TNF-α (from CD8+ and CD4+Th1) and IL-17A (from the γδ-T cell and CD4+Th17) exacerbate hypertensive responses mediating both endothelial dysfunction and cardiac, renal, and neurodegenerative injury.
The aims of this study were to investigate whether and how combined curcumin and luteolin synergistically inhibit tumor necrosis factor-alpha (TNF-α)-induced monocytes adhesion endothelium, a crucial step of the development of endothelial dysfunction, both in human vascular cells and mouse aortic endothelium.
Expression level of multiple markers implicated in inflammation (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10; metalloproteinase MMP-9) and markers of endothelial dysfunction (I-CAM and V-CAM) was determined from lung tissues mRNA using RT-PCR.
This study provides novel evidence that TNFα leads to endothelial dysfunction associated with hypertension and vascular remodeling in preeclampsia through down-regulation of endothelial nitric-oxide synthase (eNOS) by NF-κB-dependent biogenesis of microRNA (miR)-31-5p, which targets eNOS mRNA.
Unbiased hierarchical clustering identified five different clusters of sepsis mediators, including one with markers of platelet activation (e.g., thrombospondin-1) positively associated with platelet count, one with markers of inflammation (e.g., tumor necrosis factor alpha and heat shock protein 70), and endothelial dysfunction (e.g., intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) negatively associated with platelet count, and another involving growth factors of thrombopoiesis (e.g., thrombopoietin), also negatively associated with platelet count.
In contrast, DMY or blockade of miR-21 expression ameliorated endothelial dysfunction in HUVECs treated with TNF-<i>α</i> through downregulation of miR-21 expression, whereas these effects were abolished by overexpression of miR-21.
We examined the ability of metformin + esomeprazole to rescue TNF-α induced vascular cell adhesion molecule-1 (VCAM-1) and Endothelin-1 (ET-1) expression, leukocyte adhesion (markers of endothelial dysfunction).
The results of the present study demonstrated that TNF‑α was able to induce vascular endothelial dysfunction in Eahy926 cells at an optimum concentration of 10 ng/ml.
In this study, we investigated the role of receptor interacting protein 1 (RIP1), one of the kinases involved in apoptosis and necroptosis mediated by the death receptor tumor necrosis factor receptor (TNFR), in endothelial dysfunction.
We performed in vitro assays to assess whether melatonin 1) enhances the antioxidant response element genes (heme-oxygenase 1, (HO-1), glutamate-cysteine ligase (GCLC), NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1), thioredoxin (TXN)) or 2) alters secretion of the anti-angiogenic factors soluble fms-like tyrosine kinase-1 (sFLT) or soluble endoglin (sENG) from human primary trophoblasts, placental explants and human umbilical vein endothelial cells (HUVECs) and 3) can rescue TNF-α induced endothelial dysfunction.
DJC therapy exhibited a potent antioxidant activity and effectively prevented the endothelial dysfunction (ED) manifested by promoting p-eNOS expression and enhancing NO release, decreasing lipid deposition (Oil-red O staining, CPT1b and ACC) and inflammation (IL-1β, TNFα, CD68 and p-JNK), alleviating oxidative and ER stress, and decreasing the apoptosis of endothelial cells (TUNEL, BCL-2 and BAX) induced by HFD and palmitic acid respectively.
At conditions of endothelial dysfunction (ED), RES reduced the expression of cytokines, chemokines, ICAM and GM-CSF in TNF-α activated HUVECs, whereas eNOS expression was corrected to pre-ED homeostasis.
To date, there is no clear evidence that HO-1/CO prevents endothelial dysfunction associated with the downregulation of endothelial NO synthesis in human endothelial cells stimulated with TNF-α.
The aim of the study was to assess the determinants of FGF21, the correlation between FGF21 and tumor necrosis factorTNF-like weak inducer of apoptosis (sTWEAK) and the correlation between FGF21 and endothelial dysfunction in HD patients.
These findings demonstrated for the first time that BBR could prevent the oxLDL and TNFα - induced LOX1 expression and oxidative stress, key events that lead to NOX, MAPK/Erk1/2 and NF-κB activation linked to endothelial dysfunction.