The Evolving Role of Nucleotide-binding Oligomerisation Domain-like Receptor Pyrin Domain 3 Inflammasome Activation in Vascular Endothelial Cells: A Review.

In the vascular wall, defence against pathogenic damage requires a group of monocytes, the endothelium, dendritic cells, macrophages and a subsequent involvement of pattern recognition receptors anticipating damage-associated molecular patterns (DAMPs) to initiate an innate immune response. The endothelium plays a crucial role in regulating the duration, location and extent of the inflammatory cascade to ensure a definitive immune defence. Molecular changes in the expression of chemokines and cell adhesion molecules ensure protective responses against infection and injury. The multiprotein oligomer complex nucleotide-binding oligomerisation domain (NOD)-like receptor pyrin domain 3 (NLRP3) inflammasome plays a key role in the activation of inflammatory processes in response to DAMPs and pattern-associated molecular patterns. As a result of NLRP3 inflammasome activation, caspase-1 is activated and interleukin-1ß (IL-1ß) is produced. Caspase-1 is the main mediator of inflammatory feedback to tissue injury, and it is engaged both in the initiation of the inflammatory response and in the induction of cell death. NLRP3 inflammasome promotes further inflammatory responses and pyroptosis in the vascular endothelium; thus, its optimum regulation is crucial in cardiovascular homeostasis. This review outlines our current perception of the role of NLRP3 in vascular endothelial cells.

Vascular Protective Effect and Its Possible Mechanism of Action on Selected Active Phytocompounds: A Review.

Vascular endothelial dysfunction is characterized by an imbalance of vasodilation and vasoconstriction, deficiency of nitric oxide (NO) bioavailability and elevated reactive oxygen species (ROS), and proinflammatory factors. This dysfunction is a key to the early pathological development of major cardiovascular diseases including hypertension, atherosclerosis, and diabetes. Therefore, modulation of the vascular endothelium is considered an important therapeutic strategy to maintain the health of the cardiovascular system. Epidemiological studies have shown that regular consumption of medicinal plants, fruits, and vegetables promotes vascular health, lowering the risk of cardiovascular diseases. This is mainly attributed to the phytochemical compounds contained in these resources. Various databases, including Google Scholar, MEDLINE, PubMed, and the Directory of Open Access Journals, were searched to identify studies demonstrating the vascular protective effects of phytochemical compounds. The literature had revealed abundant data on phytochemical compounds protecting and improving the vascular system. Of the numerous compounds reported, curcumin, resveratrol, cyanidin-3-glucoside, berberine, epigallocatechin-3-gallate, and quercetin are discussed in this review to provide recent information on their vascular protective mechanisms in vivo and in vitro. Phytochemical compounds are promising therapeutic agents for vascular dysfunction due to their antioxidative mechanisms. However, future human studies will be necessary to confirm the clinical effects of these vascular protective mechanisms.

Cytoprotective Role of Omentin Against Oxidative Stress-Induced Vascular Endothelial Cells Injury.

Endothelial cell injury caused by reactive oxygen species (ROS) plays a critical role in the pathogenesis of cardiovascular diseases. Omentin, an adipocytokine that is abundantly expressed in visceral fat tissue, has been reported to possess anti-inflammatory and antidiabetic properties. However, endothelial protective effects of omentin against oxidative stress remain unclear. This study aimed to evaluate the protective effect of omentin against hydrogen peroxide (H2O2)-induced cell injury in human umbilical vein endothelial cells (HUVECs). Cytotoxicity and cytoprotective effects of omentin were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptotic activity of HUVECs was detected using Annexin-V/PI and Hoechst 33258 staining methods. Antioxidant activity of omentin was evaluated by measuring both reactive oxygen species (ROS) levels and glutathione peroxidase (GPx) activity. No cytotoxicity effect was observed in HUVECs treated with omentin alone at concentrations of 150 to 450 ng/ml. MTT assay showed that omentin significantly prevented the cell death induced by H2O2 (p < 0.001). Hoechst staining and flow cytometry also revealed that omentin markedly prevented H2O2-induced apoptosis. Moreover, omentin not only significantly inhibited ROS production (p < 0.01) but also significantly (p < 0.01) increased GPx activity in HUVECs. In conclusion, our data suggest that omentin may protect HUVECs from injury induced by H2O2.