Our results suggested that CaD may inhibit the expression of PTX3 by altering the IKK/IKB/NF-<i>κ</i>B pathway, thereby improving endothelial dysfunction in HUVECs.
The association of serum pentraxin-3 (PTX3) levels and endothelial dysfunction becomes a more interesting scientific research issue due to high potential of PTX3 as a diagnostic and prognostic biomarker.
We measured serum levels of biomarkers of inflammation (IL-6, IL-10, TNF-α, and hs-CRP), endothelial dysfunction (PTX3 and sTWEAK), blood-brain barrier disruption (cFN), brain damage (S100b, NSE), and trigemino-vascular activation (CGRP) by ELISA in a group of CM patients treated with OnabotA and healthy controls.
Therefore, the current study was designed to evaluate the possible role of Tanshinone IIA in influencing the expression of PTX3 in endothelial cells and thereby prevents endothelial dysfunction.
As PTX-3 is more specific than the formerly recognized biochemical markers in endothelial dysfunction, it can be used in the diagnosis of vascular originated ED.
The content or distribution of markers of endothelial dysfunction [vascular endothelial growth factor (VEGF), VEGF receptor (R) and endocan) or inflammation [intercellular adhesion molecule (ICAM)‑1, monocyte chemotactic protein (MCP)‑1 and pentraxin‑related protein (PTX3)] was evaluated via reverse transcription‑quantitative polymerase chain reaction and western blotting.
Clinical studies have so far provided contrasting results, highlighting a debated role of PTX3 as an active mediator of endothelial dysfunction, atherosclerotic plaque vulnerability and worse outcome after ischemic events.
Neutrophil overexpression of PTX3 is associated with ROS overproduction and endothelial dysfunction and may represent an emerging marker of vascular damage progression in HD patients.
In this study, we aimed to investigate the relationship of PTX-3 with circulating markers of endothelial dysfunction and atherosclerosis in patients with NAFLD.
As previous data imply that PTX3 is involved in vascular pathology and that adipose tissue mass may influence circulating PTX3 levels, we aimed to study the importance of adipose tissue expression of PTX3 in the uremic milieu and its relation to endothelial dysfunction parameters.