Search for: [Abstract = "or BaP. Supplementation of HUVEC cells with EPA or ARA and LPS activation resulted in statistically significant repression of pro\-inflammatory proteins COX\-2, cPGES \(prostaglandin E2 synthase\), and receptor for prostaglandin F2α \(FP receptor\) as well as the isoprostane 8\-isoPGF2α content. A decrease in COX\-1, COX\-2, phospholipase A2 \(cPLA2\), and toll\-like receptor 4 \(TRL4\) proteins was observed in HUVEC cells after incubation with GLA and LOVA, despite TNF\-α activation. There was an increase in the level of aromatic hydrocarbon receptor \(AHR\) after previous ARA and EPA supplementation and BaP activation, while an increase in M1 glutathione transferase \(GSTM1\) was noted only in the case of supplementation of endothelial cells with EPA and activation of BaP. Decreased mRNA levels for cytochrome P450 CYP1A1, phospholipase A2 \(PLA2G4A\), and cyclooxygenase\-2 \(prostaglandin\-endoperoxide synthase 2, PTGS2\) were evident in cells supplemented with ARA. For AHR and GSTM1 genes, significant repression of CYP1A1 was noted in PTS2A1 and PLA2G4A cells. Supplementation of HUVEC with ARA or EPA, and BaP resulted in a decrease in gene expression for VCAM\-1\(vascular cell adhesion molecule\-1\) and ICAM\-1 \(intercellular adhesion molecule\-1\) adhesion molecules. EPA supplementation of endothelial cells resulted in the highest mRNA level for the NOS3 \(nitric oxide synthase 3\) gene. In HUVEC cells"]

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