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Nigella sativa Extract and Thymoquinone Regulate Inflammatory Cytokine and TET-2 Expression in Endothelial Cells

Abstract

Numerous natural compounds including Nigella sativa (N. sativa) demonstrate anti-infammatory and anti-diabetic antiangiogenic properties. Lipopolysaccharide (LPS) mediated inflammation is regarded as an important contributor to the inflammation that is associated with the development of arteriosclerosis. In this study, it was hypothesised that N. sativa Extract (NSE) and its main active component Thymoquinone (TQ) could potentially inhibit LPS mediated inflammatory cytokine secretion and monocyte recruitment factors and monocyte in Human Vascular Endothelial Cell (HECV) lines. In addition the Ten-Eleven Translocation (TET-2) an epigenetic regulator, increasingly regarded has having a major role in both the regulation of cytokine secretion and in the development of atherosclerosis through its ability to inhibit the inflammasome Nod-like Receptor Protein 3 (NLRP3) and Interleukin-1β (IL-1β) secretion was investigated. NSE significantly inhibited the production of both IL-6 and -8 and both NSE and TQ inhibited the gene expression of vascular endothelial growth factor and monocyte chemotactic protein-1 in HECV cells. NSE and TQ inhibited the gene expression of NLRP3 and IL-1β and significantly upregulated the gene expression of TET-2 in the presence of LPS. To conclude, NSE and TQ attenuated inflammatory and monocyte recruitment response and also demonstrate a potentially important role in regulating both NLRP3 and TET-2 expression.

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Correspondence to Keith Morris.

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Peer review under responsibility of the Association for Research into Arterial Structure and Physiology

Data availability statement: All data can be made readily available through corresponding author (KM, CW and JA).

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Amartey, J., Gapper, S., Hussein, N. et al. Nigella sativa Extract and Thymoquinone Regulate Inflammatory Cytokine and TET-2 Expression in Endothelial Cells. Artery Res 25, 157–163 (2019). https://doi.org/10.2991/artres.k.191114.002

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  • DOI: https://doi.org/10.2991/artres.k.191114.002

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