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

ENDOTHELIUM physiology; INFLAMMATION prevention; ANALYSIS of variance; ANTI-inflammatory agents; BIOMARKERS; BIOLOGICAL assay; BIOLOGICAL models; BIOPHYSICS; COMPARATIVE studies; ENZYME-linked immunosorbent assay; GRAPES; RESEARCH methodology; PROSTAGLANDINS; RESEARCH funding; SEEDS; T-test (Statistics); TUMOR necrosis factors; UMBILICAL cord; VITAMIN C; WESTERN immunoblotting; PLANT extracts; OXIDATIVE stress; PHARMACODYNAMICS

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 (PG E) 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 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 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. [ABSTRACT FROM AUTHOR]