The purpose of the present study was to investigate the protective effects of salidroside against tumor necrosis factor (TNF)-α-induced vascular inflammation in cardiac microvascular endothelial cells (CMECs), a specific cell type derived from coronary micro-vessels.
This was associated with increased neutrophilic airway inflammation, vascular permeability, myeloperoxidase activity in the lung with upregulated expression of NADPH oxidase (NOX2)/MCP-1/TNF-α in neutrophils and IL-17A in γδ T cells/lung.
Thus, in conclusion, these results indicate that IL-6 trans-signaling is an important mediator of inflammation, apoptosis and barrier disruptive effects in the retinal endothelial cells and inhibition of the IL-6 trans-signaling pathway using sgp130-Fc attenuates vascular inflammation and endothelial barrier disruption.
The hypertension and vascular endothelial dysfunction evoked by subpressor doses of angiotensin II (0.25 mg·kg<sup>-1</sup> ·day<sup>-1</sup> ) were studied, and vascular inflammation was quantified by flow cytometry and real-time PCR.
These alterations were associated with higher blood pressure in humans and predisposed mice to vascular inflammation and hypertension in response to a sub-pressor dose of angiotensin II.
We investigated whether TLR 9 contributes to the development of vascular inflammation and atherogenesis using apolipoprotein E-deficient ( Apoe <sup>-/-</sup>) mice.
Increased formation of proinflammatory cytokines such as TNFα by nicotine or Copenhagen snuff may lead to vascular inflammation and thereby exacerbate atherogenesis.
Cold exposure increased the levels of gut-derived inflammatory cytokines, tumor necrosis factor-α, and interleukin-6 production in aorta and resulted in vascular inflammation, whereas atorvastatin prevented these effects.
The present study investigated the role of platelets in promoting vascular inflammation following angiotensin II (Ang II ) stimulation, and the efficacy of antiplatelet intervention.
We observed profound changes in mRNA levels for markers of tubular damage (Kim-1, NGAL) and regeneration (indirect marker of tubular injury, Ki-67), and tissue and vascular inflammation (IL-6, E-selectin, P-selectin, ICAM-1) in kidneys of PHZ-treated mice, associated with ultrastructural signs of tubular injury.
In VECs, low expression of HOXA11-AS can inhibit the expression of TNF-α-induced pro-inflammatory genes and PDGF-induced vascular inflammation-related genes.
SID suppressed the activity of cathepsin V and reversed the up-regulation of inflammatory cytokines (IL-6, IL-8 and TNF-α), adhesion and chemotaxis of leukocytes and vascular inflammation induced by l-homocysteine in vivo and in vitro.
The PTEN inhibitor inhibited the function of anti‑miR‑214 on apoptosis and inflammation in TNF‑α‑induced inflammation vascular endothelial cells through the PTEN/Akt signaling pathway.
Luteolin has been reported to possess anti-inflammatory actions and protect against tumor necrosis factor-α (TNF-α)-induced vascular inflammation, monocyte adhesion to endothelial cells and the formation of lipid-laden macrophages <i>in vitro</i>.
This established concept is based on both experimental animal models of vascular inflammation and Mendelian randomization studies demonstrating a causal relationship between pro-inflammatory cytokines (e.g. interleukin-6) and cardiovascular disease risk.
This study showed no difference over 16 weeks in vascular inflammation in patients treated with a tumor necrosis factor-α antagonist or placebo and a modest increase in vascular inflammation in carotids after 52 weeks of treatment with adalimumab.
The present study aimed to explore the protective effects of brassinin in TNF‑α‑induced vascular inflammation in human umbilical vein endothelial cells (HUVECs).