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Vitamin C blocks TNF-α-induced NF-kB activation and ICAM-1 expression in human neuroblastoma cells

Son, Eun -Wha, Mo, Sung -Ji, Rhee, Dong -Kwon, Pyo, Suhkneung
Archives of pharmacal research 2004 v.27 no.10 pp. 1073
ascorbic acid, cell adhesion, gel electrophoresis, gene expression regulation, genes, humans, inflammation, messenger RNA, necrosis, signal transduction, transcription factor NF-kappa B, tumor necrosis factor-alpha
Interactions of the cell adhesion molecules are known to play important roles in mediating inflammation. The proinflammatory cytokine, tumor necrosis factor-α (TNF-α), activates the NF-kB signaling pathway, which induces the expression of various genes, such as intercellular adhesion molecule-1 (ICAM-1). In this study, the effect of vitamin C on the ICAM-1 expression induced by TNF-α in a human neuroblastoma cell line, SK-N-SH was investigated. Treatment with vitamin C resulted in the downregulation of the TNF-α-induced surface expression and ICAM-1 mRNA levels in a concentration-dependent manner. Moreover, a gel shift analysis indicated that vitamin C dose-dependently inhibited the NF-kB activation and lkBα degradation induced by TNF-α. Taken together, these results suggest that vitamin C downregulates TNF-α-induced ICAM-1 expression via the inhibition of NF-kB activation.