dc.creator | Burja, Blaz | |
dc.creator | Kuret, Tadeja | |
dc.creator | Janko, Tea | |
dc.creator | Topalović, Dijana | |
dc.creator | Živković, Lada | |
dc.creator | Mrak-Poljsak, Katjusa | |
dc.creator | Potparević, Biljana | |
dc.creator | Zigon, Polona | |
dc.creator | Distler, Oliver | |
dc.creator | Cucnik, Sasa | |
dc.creator | Sodin-Semrl, Snezna | |
dc.creator | Lakota, Katja | |
dc.creator | Frank-Bertoncelj, Mojca | |
dc.date.accessioned | 2019-09-02T12:11:10Z | |
dc.date.available | 2019-09-02T12:11:10Z | |
dc.date.issued | 2019 | |
dc.identifier.issn | 2297-055X | |
dc.identifier.uri | https://farfar.pharmacy.bg.ac.rs/handle/123456789/3344 | |
dc.description.abstract | Olive leaf extract (OLE) is used in traditional medicine as a food supplement and as an over-the-counter drug for a variety of its effects, including anti-inflammatory and anti-atherosclerotic ones. Mechanisms through which OLE could modulate these pathways in human vasculature remain largely unknown. Serum amyloid A (SAA) plays a causal role in atherosclerosis and cardiovascular diseases and induces pro-inflammatory and pro-adhesive responses in human coronary artery endothelial cells (HCAEC). Within this study we explored whether OLE can attenuate SAA-driven responses in HCAEC. HCAEC were treated with SAA (1,000 nM) and/or OLE (0.5 and 1 mg/ml). The expression of adhesion molecules VCAM-1 and E-selectin, matrix metalloproteinases (MMP2 and MMP9) and microRNA 146a, let-7e, and let-7g (involved in the regulation of inflammation) was determined by qPCR. The amount of secreted IL-6, IL-8, MIF, and GRO-alpha in cell culture supernatants was quantified by ELISA. Phosphorylation of NF-kappa B was assessed by Western blot and DNA damage was measured using the COMET assay. OLE decreased significantly released protein levels of IL-6 and IL-8, as well as mRNA expression of E-selectin in SAA-stimulated HCAEC and reduced MMP2 levels in unstimulated cells. Phosphorylation of NF-kappa B (p65) was upregulated in the presence of SAA, with OLE significantly attenuating this SAA-induced effect. OLE stabilized SAA-induced upregulation of microRNA-146a and let-7e in HCAEC, suggesting that OLE could fine-tune the SAA-driven activity of NF-kappa B by changing the microRNA networks in HCAEC. SAA induced DNA damage and worsened the oxidative DNA damage in HCAEC, whereas OLE protected HCAEC from SAA- and H2O2-driven DNA damage. OLE significantly attenuated certain pro-inflammatory and pro-adhesive responses and decreased DNA damage in HCAEC upon stimulation with SAA. The reversal of SAA-driven endothelial activation by OLE might contribute to its anti-inflammatory and anti-atherogenic effects in HCAEC. | en |
dc.publisher | Frontiers Media Sa, Lausanne | |
dc.relation | Slovenian Research Agency - BU-RS/16-17-019 | |
dc.rights | openAccess | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.source | Frontiers in Cardiovascular Medicine | |
dc.subject | OLE | en |
dc.subject | SAA | en |
dc.subject | HCAEC | en |
dc.subject | inflammation | en |
dc.subject | atherosclerosis | en |
dc.subject | microRNA | en |
dc.subject | DNA damage | en |
dc.title | Olive Leaf Extract Attenuates Inflammatory Activation and DNA Damage in Human Arterial Endothelial Cells | en |
dc.type | article | |
dc.rights.license | BY | |
dcterms.abstract | Мрак-Пољсак, Катјуса; Зигон, Полона; Дистлер, Оливер; Бурја, Блаз; Потпаревић, Биљана; Цуцник, Саса; Живковић, Лада; Содин-Семрл, Снезна; Лакота, Катја; Топаловић, Дијана; Франк-Бертонцељ, Мојца; Курет, Тадеја; Јанко, Теа; | |
dc.citation.volume | 6 | |
dc.citation.other | 6: - | |
dc.citation.rank | M22 | |
dc.identifier.wos | 000468066500001 | |
dc.identifier.doi | 10.3389/fcvm.2019.00056 | |
dc.identifier.pmid | 31157238 | |
dc.identifier.scopus | 2-s2.0-85074985667 | |
dc.identifier.fulltext | https://farfar.pharmacy.bg.ac.rs//bitstream/id/1909/3342.pdf | |
dc.type.version | publishedVersion | |