d in the pathogenesis of atherosclerosis by promoting directed migration of inflam

Aspirin 和 Ticlopidine 抑制人類臍帶內皮細胞所表現的 趨化激素 ( 單 核球趨化激素 -1 、介白質素 -8)

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在世上是主要引起疾病和和死亡率的原因。有研究顯示在動脈硬化發 生時，細胞激素和吸附分子會促進發炎細胞的趨化。單核球趨化蛋 白 -1 (MCP-1) 是動脈硬化損傷中最早發展的一個主要因子，而 CXC 細胞激素 (IL-8) 是個有效吸引單核球到血管內皮，進而扮演增加單 核球的角色。另外，單核球吸附至內皮細胞對發炎反應是一個重要步 驟，其中包含吸附分子 (E- 選擇素 ) 的誘導。在本篇研究中，我們 探討 aspirin 和 ticlopidine 表現在人類臍帶靜脈內皮細胞 (HUVEC) 的影響。結果顯示， aspirin 以及 ticlopidine 藉由 RT-PCR 和流式細胞 分析儀抑制 TNF-α [10ng/ml] 所誘導 MCP-1 、 IL-8 以及 E- 選擇素 的表現。利用分析 MTT 試驗顯示， aspirin 和 ticlopidine 的抑制作用 並不會減少 HUVEC 生存率。這些結果顯示利用 TNF-α 刺激 HUVEC

， aspirin 以及 ticlopidine 能夠抑制 MCP-1 、 IL-8 和 E- 選擇素的釋 放，則可能提供另一項的治療機制。

Aspirin and Ticlopidine Inhibit Monocyte Chemoattractant Protein-1 、 I L-8 and E-selectin Expression

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Atherosclerosis and its complications, such as myocardial infraction, stroke, and pe

ripheral vascular disease, remain major causes of morbidity and mortality in the wo

rldwide. Studies demonstrated that chemokines and adhesion molecules are involve

d in the pathogenesis of atherosclerosis by promoting directed migration of inflam

matory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key factor

s critical for the initiation and development of atherosclerotic lesion. The CXC che

mokine, IL-8 is a powerful trigger for firm adhesion of monocyte to vascular endot

helium, indicating a potential role for this chemokine in monocyte rescruitment. M

onocyte adhesion to endothelial cells is crucial for inflammation, involving inductio

n of E-selectin. In this study, we investigated the effects of aspirin and ticlopidine o

n MCP-1 、 IL-8 and E-selectin expression in human umbilical vein endothelial cel

ls (HUVEC). Aspirin and ticlopidine inhibit TNF-α [10 ng/ml]-induced MCP-1 、 I

L-8 and E-selectin expression as detected by RT-PCR and flow cytometery. In addi

tion, the inhibitory effects of aspirin and ticlopidine were not due to decreased HU

VEC viability, as assessed by MTT test. These results suggest that aspirin and ticlo

pidine inhibit MCP-1 、 IL-8 and E-selectin release in HUVEC stimulated by TN

F-α, thereby providing an additional mechanism for therapeutic effects of aspirin an

d ticlopidine.