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目的观察银杏黄酮苷元(GA)对氧化低密度脂蛋白(ox-LDL)诱导人主动脉内皮细胞(HAECs)细胞间粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)、单核细胞趋化蛋白-1(MCP-1)的影响及核转录因子-κB(NF-κB)在其中的调控作用。方法体外培养HAECs,建立HAECs的ox-LDL损伤模型前,用不同浓度GA预处理细胞1 h,用四甲基噻唑兰法检测内皮细胞活性,免疫荧光法检测细胞核内NF-κB的激活,细胞酶联免疫吸附法检测MCP-1、ICAM-1及VCAM-1水平。结果 30~60 mg·L-1GA预处理组显著抑制ox-LDL诱导的内皮细胞NF-κB激活(P<0.05),下调VCAM-1、ICAM-1及MCP-1表达(P<0.05)。结论 GA能够有效抑制ox-LDL诱导HAECs炎症因子ICAM-1、VCAM-1、MCP-1表达。
Objective To observe the effects of ginkgetin on the expression of ICAM-1 and vascular cell adhesion molecule-1 (HAECs) induced by ox-LDL (GA) (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) and the role of nuclear factor-kappa B (NF-κB) in them. Methods HAECs were cultured in vitro. Before the establishment of HAECs model, the cells were pretreated with different concentrations of GA for 1 h. The activity of endothelial cells was detected by MTT assay. The activation of NF-κB was detected by immunofluorescence. The levels of MCP-1, ICAM-1 and VCAM-1 were detected by enzyme-linked immunosorbent assay. Results The pretreatment with 30-60 mg · L-1 GA significantly inhibited the activation of NF-κB induced by ox-LDL (P <0.05) and the expression of VCAM-1, ICAM-1 and MCP-1 in endothelial cells. Conclusion GA can effectively inhibit the expression of ICAM-1, VCAM-1 and MCP-1 in HAECs induced by ox-LDL.