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- W2368397282 abstract "Aim To investigate the effect and mechanism of ferulic acid(FA) on the expression of adhesion molecules and oxidative stress in tumor necrosis factor-α(TNF-α)-treated human umbilical vein endothelial cells(HUVEC).Methods An endothelial cell model of adhesion function damage was established by administration of TNF-α. The level of intercellular adhesion molecule-1(ICAM-1) and vascular cell adhesion molecule-1(VCAM-1) was determined by Western blot.HUVEC viability and apoptosis were detected by MTT and Hoechst 33342 staining.Reactive oxygen species(ROS) production was measured by DHE staining.Adhesion assay of monocyte and HUVEC was used to detect endothelial cell adhesive function.Nuclear factor-κB(NF-κB) activation was detected by Western blot and immunofluorescence staining.Results The TNF-α treatment caused a significant increase of ROS generation and the expression of ICAM-1 and VCAM-1 in HUVEC,which was associated with a dramatic augmentation in phosphorylation of I-κB and relocation of NF-κB into the nuclei.However,TNF-α-induced ROS generation,ICAM-1 and VCAM-1 upregulation and NF-κB relocation could be attenuated by pretreat ment of ferulic acid.Conclusion Ferulic acid could suppress TNF-α-induced adhesion molecule expression by blocking NF-κB signal and inhibiting ROS generation in HUVECs,suggesting that ferulic acid could be a novel drug candidate for the prevention and treatment of atherosclerosis." @default.
- W2368397282 created "2016-06-24" @default.
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- W2368397282 date "2013-01-01" @default.
- W2368397282 modified "2023-09-25" @default.
- W2368397282 title "Ferulic Acid Suppresses Oxidative Stress and Cell Adhesive Molecule Expression by Blocking Nuclear Factor-κB Activation in Tumor Necrosis Factor-α-Treated Human Vascular Endothelial Cells" @default.
- W2368397282 hasPublicationYear "2013" @default.
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