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目的观察银杏黄酮苷对氧化损伤的人脐静脉内皮细胞(HUVEC)产生NO、内皮型一氧化氮合酶(eNOS)和人可溶性细胞间黏附分子(ICAM-1)的影响。方法体外培养HUVEC,传至3代后,以不同浓度的银杏黄酮苷分别作用于HUVEC,然后进行氧化损伤处理。以硝酸还原酶法测定培养液上清中的NO水平,免疫细胞化学法检测内皮细胞eNOS的表达,ELISA法测定细胞培养液中ICAM-1的含量。结果HUVEC在氧化损伤(H2O2100μmol/L,2h)后产生NO的量显著减少(P<0.01),eNOS表达下调,ICAM-1表达上调;银杏黄酮苷可以剂量依赖性的增加内皮细胞NO生成量,上调eNOS的表达,下调ICAM-1表达。结论银杏黄酮苷可能通过增加HUVEC eNOS的表达增加N0的释放、抑制ICAM-1的表达等机制对内皮细胞起保护作用。
Objective To observe the effects of ginkgo flavone glycosides on NO production, endothelial nitric oxide synthase (eNOS) and human soluble intercellular adhesion molecule (ICAM-1) in oxidatively injured human umbilical vein endothelial cells (HUVEC). Methods HUVECs were cultured in vitro. After 3 passages, HUVECs were treated with different concentrations of ginkgo flavone glycosides, and then treated with oxidative damage. Nitric oxide reductase method was used to determine the level of NO in culture supernatant. The expression of eNOS in endothelial cells was detected by immunocytochemistry. The content of ICAM-1 in culture medium was determined by ELISA. Results The amount of NO produced by HUVEC after oxidative injury (H2O2100μmol/L, 2h) was significantly decreased (P<0.01), the expression of eNOS was down-regulated and the expression of ICAM-1 was up-regulated. Ginkgo biloba flavonoid glycosides could increase the NO production in endothelial cells in a dose-dependent manner. Up-regulated eNOS expression and down-regulated ICAM-1 expression. Conclusion Ginkgo biloba flavonoids may protect endothelial cells by increasing the expression of HUVEC eNOS, increasing the release of NO and inhibiting the expression of ICAM-1.