Effect of Dredging Collateral Drug on ox-LDL Injured THP-1 Cells Adhesion to Human Umbilical Vein Endothelial Cells in vitro
10.3969/j.issn.1000-3614.2016.05.015
- VernacularTitle:通络药物对血管内皮细胞与单核细胞黏附作用的影响
- Author:
Hongrong LI
;
Geng WEI
;
Ying SUN
;
Huixin LI
;
Junqing LIANG
;
Zhenhua JIA
- Publication Type:Journal Article
- Keywords:
Tongxinluo;
Ginsenoside Rb1;
Oxidative-low density lipoprotein;
Endothelium,vascular;
Monocytes
- From:
Chinese Circulation Journal
2016;31(5):480-483
- CountryChina
- Language:Chinese
-
Abstract:
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.
