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Novel molecular mechanisms by which ginger extract reduces the inflammatory stress in TNFα – activated human endothelial cells; decrease of Ninjurin-1, TNFR1 and NADPH oxidase subunits expression
- Toma, Laura, Raileanu, Mina, Deleanu, Mariana, Stancu, Camelia S., Sima, Anca V.
- Journal of functional foods 2018 v.48 pp. 654-664
- NAD(P)H oxidase (H2O2-forming), NADP (coenzyme), adhesion, advanced glycation end products, antioxidants, atherosclerosis, cell adhesion, chemokine CCL2, endothelial cells, ginger, heme oxygenase (biliverdin-producing), human cell lines, inflammation, mechanism of action, monocytes, oxidative stress, transcription factor NF-kappa B, tumor necrosis factor-alpha, vascular cell adhesion molecules
- Dysfunction of endothelial cells (EC) is important for atherosclerosis progression. The aim of this study was to evaluate the potential of ginger extract (GEx), 6-gingerol (6-G) and 6-shogaol (6-Sh) to reverse EC dysfunction and to investigate its mechanism of action, using cultured human EC incubated with TNFα. The results showed that GEx decreases monocyte chemoattractant protein-1, vascular cell adhesion molecule-1 and monocyte adhesion. This decrease was associated with the: (1) decrease of ninjurin-1 expression; (2) reduction of TNFα receptor1 and of the receptor for advanced glycation end-products expression (RAGE), in parallel with the increase of soluble RAGE; (3) decrease of NADPH oxidase subunits expression; (4) activation of antioxidant Nrf2 and heme oxygenase-1, and (5) inhibition of NF-kB. The benefic effects of 6-G and 6-Sh were weaker than those of GEx (GEx > 6-Sh > 6-G). In conclusion, GEx might be a promising alternative to ameliorate disorders in which oxidative stress and inflammation are important.