银杏黄酮苷元对ox-LDL诱导的人脐静脉内皮细胞P-选择素、LOX-1表达的影响

目的：探讨银杏黄酮苷元（ginkgetin aglycone，GA）对氧化低密度脂蛋白（oxidized-low density lipoprotein，ox-LDL）诱导的人脐静脉内皮细胞P-选择素和植物血凝素样氧化低密度脂蛋白受体-1（lectin—like oxidized low density lipoprotein receptor-1，LOX-1）表达的影响。方法：培养人脐静脉内皮细胞株ECV304，分为对照组、ox-LDL组、LOX-1拮抗剂聚肌苷酸加ox-LDL混合刺激组（聚肌苷酸组）、不同含量GA加ox-LDL混合刺激组（GA6．25mg／L组、GA12．5mg／L组、GA25mg／L组和GA50mg／L），通过逆转录聚合酶链式反应检测P-选择素mRNA和LOX-1mRNA表达，用ELISA检测各组培养基上清中P-选择素蛋白含量，辣根过氧化物酶免疫组织化学法检测LOX．1蛋白，并作比较。结果：OX-LDL上调内皮细胞P-选择素和LOX-1表达（P〈0．05）；6．25～50mg／LGA明显抑制OX-LDL诱导的内皮细胞P-选择素mRNA和LOX．1mRNA和蛋白表达（P〈0．05）；聚肌苷酸可部分或完全阻断OX-LDL诱导的内皮细胞P．选择素mRNA、LOX-1mRNA及其蛋白表达（P〈0．05）。结论：GA通过抑制LOX-1表达而降低内皮细胞合成和分泌黏附分子P-选择素，这可能是其抗动脉粥样硬化的机制之一。

Influence of ginkgetin aglycone on the expression of P-selectin and lectin-like oxidized low density lipoprotein receptor-1 induced by oxidized-low density lipoprotein in human umbilical venous endothelial cells

Objective： To investigate the effects of ginkgetin aglycone（GA） on the expression of P-selectin and lectin-like oxidized low density lipoprotein receptor-1 （LOX-1）induced by oxidized-low density lipoprotein （ox-LDL） in human umbilical venous endothelial cells. Methods： Vessel endothelial cells 304 （ECV304） were cultured, then the cells were divided into control group, ox-LDL-treated group, combining LOX-1 receptor blocker polynosinic acid（ PIA）-stimulated and ox-LDL-treated group, combining GA-stimulated（6. 25mg/L,12. 5 mg/L, 25 mg/L and 50 mg/L） and ox-LDL-treated group. RT-PCR was used to detect the expression of P-selectin mRNA and LOX-1 mRNA. P-selectin protein was measured by ELISA. LOX-1 protein level was analyzed by SP immuno- histochemistry assay. Results ： ox-LDL markedly increased the expression of P-selectin and LOX-1 in the ECV304 cells （P 〈 0. 05 ） , and 6.25 ～ 50 mg/L GA could inhibit the expression of P-selectin and LOX-1 induced by ox- LDL significantly（P 〈0. 05 ）. PIA partly or completely inhibited the expression of P-selectin mRNA, LOX-1 mRNA and its protein induced by ox-LDL in the endothelial cells（ P 〈0. 05 ）. Conclusion： GA suppresses the secretion of adhesion molecule P-selectin by inhibiting the expression of LOX-1 in endothelial cell, and it may be one of the mechanisms of anti-atherosclerosis.