[Effect of Huoxue injection on oxidized low-density lipoprotein induced activation of human umbilical vein endothelial cells].

Objective:To observe effect of Huoxue injection on the expression of intercellular cell adhesion molecule-1 (ICAM-1)and vascular cell adhesion molecule-1(VCAM-1),the adherence of monocytes to endothelial cells,and the regulation role of nuclear factor kappa B(NF-(?)B)in cultured human umbilical vein endothelial cells(HUVEC)injury induced by the oxidized low- density lipoprotein(ox-LDL).Method:The ox-LDL(100 mg·L~(-1))was added to the cultured HUVEC to prepare the injury model of HUVEC.The adhesive percentage between HUVEC treated with ox-LDL and monocytes was determined by protein quantification. Expression of mRNA and protein of ICAM-1 and VCAM-1 were determined by RT-PCR and flow cytometry respectively.The percentage of positive cells and the ratio of nuclei and cytoplasm of NF-(?)B p65 staining in HUVEC the were examined by cell immunochemistry. Result:Treatment of HUVEC with ox-LDL for 12,24 hours significantly increased adhesion of monocytes to HUVEC and enhanced the expressions of mRNA and protein of ICAM-1 and VCAM-1.The percentage of positive cells and the ratio of nuclei and cytoplasm of NF-(?)B p65 staining in HUVEC were significantly increased after treatment with ox-LDL for 24 hours.Huo Xue Injection could signifi- cantly inhibit the adhesion between monocyte and HUVEC,the expression of mRNA and protein of ICAM-1 and VCAM-1,and de- clined the percentage of positive cells and the ratio of nuclei and cytoplasm of NF-(?)B p65 staining in HUVEC.The effects were strengthened with increasing the deal of Huoxue injection.Conclusion:Huoxue injection has an inhibitory effect on the adherence of monocytes to HUVEC,probably by way of down-regulating the expression of mRNA and protein of ICAM-1 and VCAM-1 in HUVEC. The mechanism is probably associated with inhibiting the activation of NF-(?)B p65 of HUVEC.The effects of Huoxue injection can bring about the protective effect to endothelial cells injury induced by ox-LDL.