中文摘要：

肿瘤坏死因素 --(TNF-) 并且 monocytic 房间在动脉粥样硬化的发展起一个关键作用，它是冠的心疾病(CHD ) 的主要原因。在这个工作，我们在血在单核白血球上调查了过量 TNF- 的效果并且发现从 CHD 病人的血单核白血球有潜力直接形成 cholesteryl 酉旨(CE ) 沉重的房间在下面在里面有 oxLDL 的 vitro 孵化。proinflammatory cytokines 的血浆层次例如 TNF- ， interleukin 6 (IL-6 ) ，并且 C 反应蛋白质(CRP ) ，在 CHD，病人们是比在控制的那些显著地高级的健康志愿者。然而， TNF- ，然而并非 IL-6 或 CRP 的仅仅血浆水平，断然与血单核白血球的潜力被相关直接形成 CE 沉重的房间。由使用人的血单核白血球和 monocytic THP-1 房间， CE 沉重的房间的形成上的 TNF- 的激活的效果被表明，它能被 anti-TNF- 抗体明确地堵住。而且， TNF- 能由分别地提高功能的粘附分子和 scavenger 受体的表示增加粘附和单核白血球的 oxLDL 举起，这也被揭示。最后，结果在 vivo 并且在 vitro，与一个老鼠模型一起的实验证实在血的过量 TNF- 与潜力激活单核白血球直接形成 CE 沉重的房间。这些数据证明在血的过量 TNF- 是为动脉粥样硬化和 CHD 的开发的主要扳机。

英文摘要：

The tumor necrosis factor-α （TNF-α） and monocytic cells play a critical role in the development of ath- erosclerosis, which is the major cause of coronary heart disease （CHD）. In this work, we investigated the effect of excess TNF-α on monocytes in the blood and found that blood monocytes from the CHD pa- tients had the potential to directly form cholesteryl ester （CE）-Iaden cells under the in vitro incubation with oxLDL. The plasma levels of proinflammatory cytokines, such as TNF-α, interleukin 6 （IL-6）, and C reactive protein （CRP）, in the CHD patients were significantly higher than those in the control healthy volunteers. However, only the plasma level of TNF-α, but not of IL-6 or CRP, is positively correlated with the potential of blood monocytes to directly form CE-laden cells. By using human blood mono- cytes and monocytic THP-1 cells, the activating effect of TNF-α on the formation of the CE-laden cells was demonstrated, which could be specifically blocked by the anti-TNF-α antibody. Furthermore, it was also revealed that TNF-α could boost adhesion and oxLDL uptake of the monocytes by enhancing the expression of the functional adhesion molecules and scavenger receptors, respectively. Finally, the re- sults of in vivo and in vitro experiments with a mouse model confirmed that excess TNF-α in the blood activates monocytes with the potential to directly form CE-laden cells. These data demonstrate that excess TNF-α in the blood is the primary trigger for the development of atherosclerosis and CHD.