Son Eun-Wha, Mo Sung-Ji, Rhee Dong-Kwon, Pyo Suhkneung
Dept. of Pharmacognosy Material Development, Samcheok National University, Samcheok, Kangwon-do 245-711, Korea.
Arch Pharm Res. 2004 Oct;27(10):1073-9.
Interactions of the cell adhesion molecules are known to play important roles in mediating inflammation. The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), activates the NF-kappaB 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-alpha in a human neuroblastoma cell line, SK-N-SH was investigated. Treatment with vitamin C resulted in the downregulation of the TNF-alpha-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-kappaB activation and IkappaBalpha degradation induced by TNF-alpha. Taken together, these results suggest that vitamin C downregulates TNF-alpha-induced ICAM-1 expression via the inhibition of NF-kappaB activation.
已知细胞粘附分子的相互作用在介导炎症中起重要作用。促炎细胞因子肿瘤坏死因子-α（TNF-α）激活NF-κB信号通路，该通路诱导各种基因的表达，如细胞间粘附分子-1（ICAM-1）。在本研究中，研究了维生素C对人神经母细胞瘤细胞系SK-N-SH中TNF-α诱导的ICAM-1表达的影响。维生素C处理导致TNF-α诱导的表面表达和ICAM-1 mRNA水平以浓度依赖性方式下调。此外，凝胶迁移分析表明维生素C剂量依赖性地抑制TNF-α诱导的NF-κB激活和IκBα降解。综上所述，这些结果表明维生素C通过抑制NF-κB激活下调TNF-α诱导的ICAM-1表达。
