Grape seed extract ameliorates tumor necrosis factor-α-induced inflammatory status of human umbilical vein endothelial cells

Chia-Lun Chao, Nen-Chung Chang, Ching-Sung Weng, Kueir-Rarn Lee, Shung-Te Kao, Jiin-Chyr Hsu, Feng-Ming Ho
European Journal of Nutrition 2011, 50 (6): 401-9

BACKGROUND: Inflammation has played a key role in the causation of atherosclerosis. However, the effects of grape seed extract (GSE) on the pro-inflammatory intracellular signaling, enzyme activity, and inflammatory mediators of endothelial cells have not been sufficiently studied, and less information exists on the comparison between GSE and vitamin C, a well-known antioxidant compound, on their anti-inflammatory properties.

PURPOSE: We investigated the effects of GSE and vitamin C on the cell viability, oxidative stress, monocyte adhesion, the expression of nuclear factor-κB inhibitor (IκB), intercellular adhesion molecule-1 (ICAM-1) and cyclooxygenase-2 (COX-2), and the production of prostaglandin E(2) (PG E(2)) in TNF-α-treated human umbilical vein endothelial cells (HUVECs).

METHODS: Cell viability was measured by MTT assay. The adhesion of THP-1 to HUVECs was evaluated by cell adhesion assay. The oxidized nucleoside 8-hydroxydeoxyguanosine (8-OHdG) (an indicator of oxidative damage to DNA), ICAM-1, and PG E(2) were measured by ELISA. IκB and COX-2 expression were evaluated by western blot analysis.

RESULTS: TNF-α (10, 20, and 50 ng/mL), GSE (50 and 200 μg/mL), or vitamin C (100 μM) did not affect cell viability. GSE (50-100 μg/mL) attenuated TNF-α (20 ng/mL)-induced 8-OHdG production, THP-1 adhesion, the expression of IκB degradation, ICAM-1 and COX-2, and the production of PGE(2) in a dose-dependent manner. Vitamin C (100 μM) also showed significant antioxidative and anti-inflammatory effects.

CONCLUSIONS: GSE effectively ameliorates TNF-α-induced inflammatory status of HUVECs. The findings of the present study suggest that consumption of GSE may be beneficial to inflammatory atherosclerosis.

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