三七总皂苷对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞的细胞间黏附分子-1的影响

目的 研究三七总皂苷对氧化型低密度脂蛋白(ox LDL )损伤血管内皮细胞的保护作用,以探讨其治疗动脉硬化闭塞症 (ASO)的机制。方法 以培养原代人脐静脉内皮细胞（HUVEC）作为靶细胞, 用ox LDL造成HUVEC损伤模型，以三七总皂苷进行干预。光镜下观察细胞形态变化,MTT法检测细胞活性；采用蛋白定量法检测HUVEC与单核细胞的黏附率；用流式细胞仪测定HUVEC的细胞间黏附分子-1（ICAM-1）的蛋白表达。结果 ox-LDL作用HUVEC后12、24 h时，HUVEC损伤明显，细胞活性显著降低，人单核细胞与HUVEC的黏附率显著升高, HUVEC的ICAM 1的蛋白表达水平也明显升高, 均明显高于正常对照组(P＜0.05，P＜0.01),而三七总皂苷能使ox-LDL损伤的HUVEC形态趋于正常,活性增强，并明显降低人单核细胞与HUVEC的黏附率，显著降低ICAM-1蛋白的表达水平，与ox-LDL组比较差异有统计学意义(P＜0.05，P＜0.01)，这种作用随着剂量的增加而增强。结论 三七总皂苷能通过下调内皮细胞表面黏附分子的表达抑制单核－血管内皮细胞黏附,从而发挥对血管内皮细胞的保护作用，这可能是其治疗ASO的机制之一。

Effects of Panax Notoginseng Saponins on Expression of Intercellular Adhesion Molecule-1 in Human Umbilical Vein Endothelial Cells Injury Induced by Oxidized Low-density Lipoprotein

Objective To study the protective effect of panax notoginseng saponins (PNS) on human umbili- cal vascular endothelial cells (HUVECs) injury induced by oxidized low-density lipoprotein (ox-LDL) for investi- gating the mechanism of PNS in treating arteriosclerosis obliterans (ASO).Methods Taking the cultured HU- VECs as target cells,ox-LDL was used to establish a model of injured HUVEC and it was then intervened by PNS. The morphologic changes of HUVEC were observed under light microscope;activity of cells was determined by MTT method;the adhesive percentage between ox-LDL treated HUVEC and monocyte determined by protein quantifica- tion and the protein expression of intercellular adhesion molecule-1 (ICAM-1) determined by flow cytometry.Re- suits At the time points of HUVEC being treated with ox-LDL (100 mg/L) for 12 h and 24 h,significant injury of HUVEC was shown,its activity reduced,the adhesion rate with monocytes elevated,and the protein expression of ICAM-1 in HUVEC increased significantly (P<0.05,P<0.01).PNS showed significant effect in reversing all the above changes,as compared with the control group (without PNS treaded),respective significant difference was shown in all the four indexes (P<0.05,P<0.01).Conclusion PNS has a protective effect on endothelial cells injury induced by ox-LDL,which may be one of its mechanisms in treating ASO.The protective effect of PNS is probably by way of down-regulating the expression of ICAM-1 in endothelial cells and inhibiting the adherence of monocytes to endothelial cells.