穿心蓮內酯對腫瘤壞死因子誘發EA.hy926細胞中細胞黏著分子表現之影響

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题名:	穿心蓮內酯對腫瘤壞死因子誘發EA.hy926細胞中細胞黏著分子表現之影響 Effect of andrographolide on tumor necrosis factor-alpha-induced intercellular adhesion molecule-1 expression in EA.hy926 cells
作者:	蔡伊婷;I-Ting Tsai
贡献者:	健康照護學院營養學系碩士班
关键词:	穿心蓮內酯;腫瘤壞死因子;細胞間黏著分子-1;nuclear factor-kappa B (NF-κB);EA.hy926 cells;andrographolide;tumor necrosis factor-α;intercellular adhesion molecule-1;nuclear factor-kappa B;EA.hy926 cells
日期:	2010
上传时间:	2010-09-29 12:09:42 (UTC+8)
摘要:	許多研究顯示，發炎反應及血管內皮細胞功能異常為動脈粥狀硬化起始的關鍵。腫瘤壞死因子 (tumor necrosis factor-α, TNF-α) 為重要的促發炎細胞激素，它會促進內皮細胞中黏著分子的表現，使單核球黏附至內皮細胞上，進而形成動脈粥狀硬化斑塊。穿心蓮 (Andrographis paniculata) 中的活性成分穿心蓮內酯 (andrographolide) 被證實具有抗發炎作用。本研究以人類內皮細胞EA.hy926來探討穿心蓮內酯對腫瘤壞死因子所誘發的細胞黏著分子-1 (intercellular adhesion molecule, ICAM-1) 基因表現之影響。研究結果發現，穿心蓮內酯除了能抑制腫瘤壞死因子所誘發的ICAM-1 mRNA、蛋白質及其在細胞膜表面之表現，亦能抑制腫瘤壞死因子所誘發EA.hy926細胞與單核球HL-60細胞的黏附作用。進一步探討發現，穿心蓮內酯會降低腫瘤壞死因子所誘發的κB inhibitor (IκB) kinase (IKK) 及IκBα活化、減少p65進入細胞核內、降低NF-κB與DNA的結合，並且減少ICAM-1報導基因活性。另外研究結果發現，穿心蓮內酯能增加胞內cAMP濃度並活化cAMP response element-binding protein (CREB)，但在knockdown CREB的表現下，穿心蓮內酯抑制腫瘤壞死因子所誘發的ICAM-1表現並不受影響。本研究證實在EA.hy926細胞中，穿心蓮內酯會藉由減少NF-κB活化，進而抑制腫瘤壞死因子所誘發的ICAM-1表現。此研究結果意謂穿心蓮具有預防動脈粥狀硬化發生的潛力。 Several lines of evidence indicate that inflammation and endothelial cell dysfunction are important initiating events in atherosclerosis. Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, induces the expression of cell adhesion molecules and results in monocyte adherence and atheromatous plaques formation. Andrographolide (AP) is a major bioactive diterpene lactone in Andrographis paniculata, which possesses anti-inflammatory property. In the present study, we investigated the effect of AP on TNF-α-induced ICAM-1 expression in EA.hy926 cells. AP inhibited TNF-α-induced ICAM-1 mRNA, total protein, and cell-surface expressions. In addition, TNF-α-induced adhesion of HL-60 to EA.hy926 cells was abolished by AP. Furthermore, AP suppressed TNF-α-induced κB inhibitor (IκB) kinase (IKK) and IκBα activation, p65 nuclear translocation, NF-κB and DNA binding activity, and promoter activity of ICAM-1. AP increased intracellular cAMP concentration and induced the phosphorylation of cAMP response element-binding protein (CREB). Transfection with CREB-specific small interfering RNA knocked down CREB expression, however, did not inhibit ICAM-1 expression by AP. Taken together, these results suggest that AP down-regulates TNF-α-induced ICAM-1 expression via attenuation of activation of NF-κB in EA.hy926 cells. The results may implicate the cardiovascular-protective potential of AP.
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