Arnould T, Michiels C, Janssens D, Berna N, Remacle J
Laboratoire de Biochimie et Biologie Cellulaire, Facultés Universitaires Notre-Dame de la Paix, Namur, Belgium.
J Cardiovasc Pharmacol. 1998 Mar;31(3):456-63. doi: 10.1097/00005344-199803000-00018.
This study was performed to evaluate the effects of Ginkor Fort, a venotropic drug composed of Ginkgo biloba extract, troxerutine, and heptaminol, on neutrophil adherence to the endothelium of saphenous veins. When saphenous veins were incubated 2 h in hypoxic conditions, they showed a five- to sixfold increase in neutrophil adherence to the endothelium. Ginkor Fort at 0.3 mg/ml was able to inhibit this increase by 69%. These results were confirmed by observations in scanning electron microscopy. Ginkor Fort also inhibited the subsequent activation of these neutrophils, as evidenced by the inhibition of superoxide anion release. The biochemical mechanism of this inhibition of neutrophil adherence was studied on endothelial cells in culture. We observed that Ginkor Fort was able to inhibit the different steps of the activation of endothelial cells by hypoxia: the activation of phospholipase A2 and the decrease in adenosine triphosphate (ATP) content. By preventing the first step of the activation cascade, the decrease in ATP content, Ginkor Fort blocks the subsequent increase in neutrophil adherence as well as neutrophil activation. The biochemical mechanism evidenced in this work might explain the beneficial effect of this drug in the treatment of patients with chronic venous insufficiency.
本研究旨在评估金纳多复方制剂（一种由银杏叶提取物、曲克芦丁和庚胺醇组成的血管趋向性药物）对中性粒细胞黏附于隐静脉内皮的影响。当隐静脉在缺氧条件下孵育2小时后，中性粒细胞对内皮的黏附增加了五到六倍。浓度为0.3mg/ml的金纳多复方制剂能够抑制这种增加，抑制率达69%。扫描电子显微镜观察结果证实了这些发现。金纳多复方制剂还抑制了这些中性粒细胞随后的活化，这可通过超氧阴离子释放的抑制得到证明。在培养的内皮细胞上研究了这种抑制中性粒细胞黏附的生化机制。我们观察到，金纳多复方制剂能够抑制缺氧对内皮细胞活化的不同步骤：磷脂酶A2的活化以及三磷酸腺苷（ATP）含量的降低。通过阻止活化级联反应的第一步，即ATP含量的降低，金纳多复方制剂阻断了随后中性粒细胞黏附的增加以及中性粒细胞的活化。这项研究中证实的生化机制可能解释了这种药物在治疗慢性静脉功能不全患者中的有益作用。
