Objective: To observe the effect of oxidative-low density lipoprotein (ox-LDL) injured human leukemia mononuclear cells (THP-1) adhesion to human umbilical vein endothelial cells (HUVECs)in vitrowith the intervening function of dredging collateral drug, tongxinluo (TXL) and ginsenoside (Rb1). Methods: Cell injury was induced by ox-LDL treatment. The cells were divided into 4 groups:①Normal control group,②Injury model group, the cells were cultured by ox-LDL,③TXL group, the cells were cultured with both ox-LDL and TXL,④Rb1 group. HUVEC viability was measured by MTS assay, adherence rate of THP-1 cells to HUVECs was tested by vital cell staining. The contents of monocyte chemoat-tractant protein (MCP-1), soluble vascular cell adhesion molecule (sVCAM-1), soluble inter vascular cell adhesion molecule-1 (sICAM-1) and E-selectin in HUVEC conditioned medium were detected by ELISA; protein expressions of CCR2, VLA4 and Mac-1 in THP-1 cells were examined by Western blot analysis. Results: Compared with Control group, HUVEC viability was decreased in Injury model group (100 ±1.31) % vs(75.57 ± 1.02) %, while increased in both TXL and Rb1 groups (99.25 ± 1.40) % and (99.48 ± 2.15) %; Injury model group showed elevated adherence rate of THP-1 cells to HUVECs, while the adherence rates were reduced in both TXL and Rb1 groups. Compared with Injury model group, TXL group and Rb1 group showed decreased levels of MCP-1, sVCAM-1, sICAM-1 and E-selectin in HUVEC conditioned medium; decreased protein expressions of CCR2, VLA4 and Mac-1 in THP-1 cells. Conclusion: TXL and Rb1 could protect HUVECs, reduce ox-LDL injury induced vascular endothelial cell adhesion and decrease relevant receptor expression in monocytes; therefore, inhibit injured monocytes adherence to vascular endothelial cells.%目的：观察氧化低密度脂蛋白（ox-LDL）损伤的血管内皮细胞（HUVEC）与人白血病单核细胞（THP-1）的黏附作用，以及通络药物（通心络超微粉溶液和人参皂苷Rb1）干预的影响。方法：采用ox-LDL建立血管内皮细胞损伤模型，将细胞分为正常对照组、模型组、通心络组和人参皂苷Rb1组。实验采用MTS比色法检测ox-LDL损伤的HUVEC的生存活性，用活细胞染色方法观察不同组HUVEC与THP-1细胞的黏附率，用酶联免疫吸附测定（ELISA）方法检测HUVEC培养上清中单核细胞趋化因子（MCP-1）、可溶性血管内皮细胞间黏附分子（sVCAM-1）、可溶性内皮细胞间黏附分子（sICAM-1）、E-选择素（E-selectin）的水平，用蛋白免疫印迹法（Western Blot）检测各组HUVEC条件培养基培养的单核细胞趋化因子受体2（CCR2）、极迟抗原4（VLA-4）、巨噬细胞分化抗原-1（Mac-1）的表达。结果：与正常对照组（100.00±1.31）%比较，模型组HUVEC生存活性降低为正常对照组的（75.57±1.02）%，通心络组和人参皂苷Rb1组HUVEC生存活性明显分别提高了（99.25±1.40）%、（99.48±2.15）%。与正常对照组比较，模型组黏附于HUVEC的THP-1细胞数量明显增多，与模型组比较，通心络组和人参皂苷Rb1组黏附于HUVEC细胞的THP-1细胞数量减少。通心络组和人参皂苷Rb1组HUVEC细胞培养上清中MCP-1、sVCAM-1、sICAM-1、E-selectin的水平和THP-1细胞上相应受体CCR2、VLA-4、Mac-1的表达较模型组降低。上述比较差异均有统计学意义（P<0.05）。结论：通心络和人参皂苷Rb1能够保护HUVEC，减少ox-LDL损伤的血管内皮细胞趋化、黏附分子的分泌及单核细胞上相应受体的表达，从而抑制单核细胞向受损血管内皮的趋化黏附。
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