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作 者:何艳[1] 付永昕[1,2] 吴立荣[1] 刘兴德[1] 方颖[1] 李屏[1] 李安敏[1] 陈云[1]
机构地区:[1]贵阳医学院附属医院心内科,550001 [2]重庆市第三人民医院,400014
出 处:《新医学》2009年第10期647-650,共4页Journal of New Medicine
基 金:贵州省优秀科技教育人才省长专项资金项目(黔省专合字225号)
摘 要: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。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.
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