凝血接触系统对人血管内皮细胞炎症活性的影响

The Effects of Coagulation Contact System on Human Vascular Endothelial Cells

内源性凝血途径的起始部分称为接触系统,包括高分子量激肽原、前激肽释放酶、XII因子和XI因子。以接触系统成分及激活产物分别刺激人血管内皮细胞,检测了其NF-κB活性、细胞间黏附分子1(ICAM-1)表达和炎性细胞因子分泌的变化。结果显示:与对照组相比较,只有游离XI因子和激活的XI因子可以使内皮细胞NF-κB活性升高,并具有统计学差异(P<0.01);而激活的XI因子能够进一步使内皮细胞的ICAM-1和细胞因子分泌显著增加(P<0.01)。其余各组与对照组相比没有统计学差异。这些观察结果提示接触系统可以直接活化血管内皮细胞,说明内源性凝血途径也参与了炎症的发展过程。

Contact system is the beginning of intrinsic coagulation pathway and comprises four components： high molecular weight kininogen, prekallikrein, factor Ⅻ （FXII） and factor Ⅺ （FXI）. We detected the NF-κB activity, expression of intercellular adhesion molecule- 1 （ICAM- 1） and secretion of TNF-α IL-2, IL-6 of EA.hy926 （derived form human umbilical vein endothelium） which was stimulated by the components and products of contact system to reveal the impact of intrinsic coagulation pathway on inflammation. We found that compared with the control group, only free factor Ⅺ and activated FXI （FXIa） could up-regulate NF-κB activity （P〈0.01）; FXIa could further up-regulate expression of ICAM-1 on cells membrane （P〈0.01） and secretion of inflammatory cytokines. There is no statistic difference between other groups. These findings indicate that FXI and FXIa have directly influences on endothelium status, which means that intrinsic coagulation pathway contributes the development of inflammation like extrinsic pathway does.