Sulforaphane inhibits TNF-α-induced activation of p38 MAP kinase and VCAM-1 and MCP-1 expression in endothelial cells
Sulforaphane inhibits TNF-α-induced activation of p38 MAP kinase and VCAM-1 and MCP-1 expression in endothelial cells
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DOI：
10.1007/s00011-009-0017-7
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发表时间：
2009-08-01
影响因子：
6.7
通讯作者：
Kunsch, Charles
中科院分区：
文献类型：
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作者：
Chen, Xi-Lin;Dodd, Geraldine;Kunsch, Charles
为探讨莱菔硫烷对内皮细胞炎症基因表达的影响，以人主动脉内皮细胞为材料，用莱菔硫烷（1-4 μ M）预处理内皮细胞1小时，可抑制TNF-α诱导的MCP-1和VCAM-1的mRNA和蛋白水平，但对TNF-α诱导的ICAM-1表达无影响。萝卜硫素还抑制TNF-α诱导的p38 MAP激酶的激活，但不抑制c-Jun-N-末端激酶。莱菔硫烷对TNF-α诱导的NF-κ B B核结合活性、I κ B-α降解或NF-κ B驱动的转录活性的激活没有影响。显性负性Nrf 2的表达抑制了萝卜硫素诱导的抗氧化反应元件（ARE）驱动的启动子活性，但对萝卜硫素介导的VCAM-1和MCP-1表达的抑制没有影响。
To investigate the effects of sulforaphane on endothelial inflammatory gene expression in endothelial cells.Human aortic endothelial cells were used in the study.One-hour pretreatment of endothelial cells (EC) with sulforaphane (1-4 mu M) suppressed TNF-alpha-induced MCP-1 and VCAM-1 mRNA and protein levels, but had no effect on TNF-alpha-induced ICAM-1 expression. Sulforaphane also inhibited TNF-alpha-induced activation of p38 MAP kinase, but not c-Jun-N-terminal kinase. Sulforaphane had no effect on TNF-alpha-induced NF-kappa B nuclear binding activity, I kappa B-alpha degradation or activation of NF-kappa B-driven transcriptional activity. Expression of dominant negative Nrf2 inhibited sulforaphane-induced antioxidant response element (ARE)-driven promoter activity, but had no effect on sulforaphane-mediated inhibition of VCAM-1 and MCP-1 expression.These data suggest that sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.