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Tytuł pozycji:

Therapeutic role of eicosapentaenoic and arachidonic acid in benzo(a) pyrene-induced toxicity in HUVEC endothelial cells.

Tytuł:
Therapeutic role of eicosapentaenoic and arachidonic acid in benzo(a) pyrene-induced toxicity in HUVEC endothelial cells.
Autorzy:
Sroczyńska K; Department of Radioligands, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688 Kraków, Poland.
Totoń-Żurańska J; Center for Medical Genomics - OMICRON, Jagiellonian University Medical College, M. Kopernika 7c, 31-034 Krakow, Poland.
Czepiel J; Department of Infectious and Tropical Diseases, Faculty of Medicine, Jagiellonian University Medical College, M. Jakubowskiego 2, 30-688 Krakow, Poland.
Zając-Grabiec A; Department of Radioligands, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688 Kraków, Poland.
Jurczyszyn A; Department of Hematology, University Hospital, M. Kopernika 17, 31-501 Kraków, Poland.
Wołkow P; Center for Medical Genomics - OMICRON, Jagiellonian University Medical College, M. Kopernika 7c, 31-034 Krakow, Poland.
Librowski T; Department of Radioligands, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688 Kraków, Poland.
Gdula-Argasińska J; Department of Radioligands, Faculty of Pharmacy, Jagiellonian University, Medical College, Medyczna 9, 30-688 Kraków, Poland. Electronic address: .
Źródło:
Life sciences [Life Sci] 2022 Mar 15; Vol. 293, pp. 120345. Date of Electronic Publication: 2022 Jan 20.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
MeSH Terms:
Arachidonic Acid/*pharmacology
Benzo(a)pyrene/*toxicity
Cell Survival/*drug effects
Eicosapentaenoic Acid/*pharmacology
Human Umbilical Vein Endothelial Cells/*drug effects
Human Umbilical Vein Endothelial Cells/*metabolism
Cell Survival/physiology ; Cytochrome P-450 CYP1A1/metabolism ; Dose-Response Relationship, Drug ; Humans
Contributed Indexing:
Keywords: Arachidonic acid; Benzo(a)pyrene; Eicosapentaenoic acid; HUVEC endothelial cells; Inflammation
Substance Nomenclature:
27YG812J1I (Arachidonic Acid)
3417WMA06D (Benzo(a)pyrene)
AAN7QOV9EA (Eicosapentaenoic Acid)
EC 1.14.14.1 (CYP1A1 protein, human)
EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
Entry Date(s):
Date Created: 20220122 Date Completed: 20220221 Latest Revision: 20220221
Update Code:
20240105
DOI:
10.1016/j.lfs.2022.120345
PMID:
35065163
Czasopismo naukowe
Endothelial cells are characterized by intense metabolic activity and control of homeostasis. Exposure to benzo(a)pyrene (BaP) plays an important role in the etiology of atherosclerosis. The study aimed to determine the effect of arachidonic (ARA), and eicosapentaenoic acid (EPA) on pro-inflammatory gene and protein levels in human umbilical vein endothelial cells (HUVEC) exposed to BaP. Cyclooxygenase-2 (COX-2), aryl hydrocarbon receptor (AHR), and glutathione S transferase Mu1 (GSTM1) proteins expression were analyzed by Western blot. Prostaglandin synthase 2 (PTGS2), AHR, GSTM1, phospholipase A2 (PLA2G4A), cytochrome P450 CYP1A1, intercellular adhesion molecule-1 (ICAM-1), endothelial nitric-oxide synthase (NOS3), and vascular adhesion molecule-1 gene expression (VCAM-1) was analyzed in Real time-qPCR. Phospholipase A2 activity was measured using the ELISA technique, and CYP1A1 activity was analyzed in luminescence assay. The highest amount of COX-2, the most increased activity of CYP1A1 and cPLA2, and overexpression of GSTM1, CYP1A1, ICAM-1, and VCAM-1 gene was observed in HUVEC cells treated with BaP. After co-treatment with BaP and ARA or EPA, an increase of GSTM1 level was observed. Incubation of endothelial cells with ARA or EPA and BaP resulted in lower CYP1A1 and cPLA2 activities and lower expression of VCAM-1 and ICAM-1 genes. Significant overexpression of AHR, GSTM1, CYP1A1, PTGS2, PLA2G4A, and NOS3 genes was noted in cells treated with EPA and BaP. Our data suggest a beneficial effect of EPA and ARA on endothelial function. Thus, it justifies further research on the participation of fatty acids in the regulation of physiological and pathological processes in endothelial cells.
(Copyright © 2022 Elsevier Inc. All rights reserved.)

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