1. TNF©\¦Á induces mRNA expression of IL©\8 and MCP©\1 in the cells.
2. Vitamin C blocks TNF-alpha-induced NF-kappaB activation and ICAM-1 expression in human neuroblastoma cells
Vitamin C blocks TNF-alpha-induced NF-kappaB activation and ICAM-1 expression in human neuroblastoma cells
Eun-Wha Son, Sung-Ji Mo1, Dong-Kwon Rhee1, and Suhkneung Pyo1Dept. of Pharmacognosy Material Development, Samcheok National University, Samcheok, Kangwon-do 245-711,Korea and 1Division of Immunopharmacology, College of Pharmacy, Sungkyunkwan University, Suwon, Kyunggi-do
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.
Effect of vitamin C on TNF-¦Á-induced ICAM-1 ex-pression in neuroblastoma cells
It has previously been shown that some cytokinesinduce the expression of adhesion molecules on neuronalcells and facilitate the adherence of leukocytes (Birdsall,et al., 1992). To establish if TNF-¦Á induced the expressionof ICAM-1 on neuroblastoma cells, the levels of ICAM-1on the surface of these cells was examined. As shown inFig. 1, the ICAM-1 expression was constitutively expressedon SK-N-SH cells, and the treatment of SK-N-SH cellswith TNF-¦Á increased the expression of ICAM-1.The effect of vitamin C on the TNF-¦Á stimulates The experiments described above demonstrated thatvitamin C markedly inhibits the cell surface expression ofICAM-1 in cells stimulated with TNF-¦Á. It was possiblethat the interference of vitamin C with TNF-¦Á-induced ICAM-1 upregulation also occurs at the transcriptional level. Toaddress this possibility, and measure the reproducibility ofthe ELISA analysis, total cellular RNAs were isolated fromcells and analyzed by RT-PCR. Cells were pretreated withvarious doses of vitamin C for 1 h, and then stimulatedwith TNF-¦Á for 4 h. Treatment with vitamin C markedlydecreased the induction of ICAM-1 mRNAs (Fig. 2B). Thelevel of mRNA inhibition appeared comparable with that of the surface expression inhibition.
Inhibition of TNF-¦Á-induced activation of NF-kBand degradation of IkBs by vitamin C
Vitamin C Acid Blocks TNF-¦Á-induced NF-kB Activation
(PDF) Vitamin C blocks TNF-alpha-induced NF-kappaB activation and ICAM-1 expression in human neuroblastoma cells
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Dec 21, 2018 ¡¤ Vitamin C is a NFkB inhibitor, which means it plays a key role in the inhibition of inflammation in the body and skin. This is important for inflammatory skin conditions like acne vulgaris and rosacea. Vitamin C can have a positive effect to reduce the inflammation associated with these conditions. STABILITY VS. BIOAVAILABILITY