银杏内酯B对血小板活化因子刺激的大鼠中性粒细胞功能的影响银杏内酯B对血小板活化因子刺激的大鼠中性粒细胞功能的影响

目的 研究银杏内酯B对血小板活化因子(PAF)刺激的大鼠中性粒细胞粘附、趋化及脱颗粒功能的影响。方法 从大鼠外周血分离中性粒细胞,用MTT比色法、Boyden小室法及β-葡萄糖苷酸酶释放法分别检测PAF诱导的粒细胞粘附、趋化及脱颗粒反应。结果10 μmol·L^-1 银杏内酯B可显著抑制中性粒细胞的粘附反应;1～1 000 nmol·L^-1 可剂量依赖性抑制10 nmol·L^-1 PAF诱发的粒细胞趋化反应,其IC₅₀为4.84 nmol·L^-1; 0.01～10 μmol·L^-1可抑制1 μmol·L^-1 PAF诱发的粒细胞释放β-葡糖苷酸酶,其IC₅₀为3.56 μmol·L^-1。结论银杏内酯B能够抑制PAF刺激的大鼠中性粒细胞粘附、趋化及脱颗粒反应。

Effect of ginkgolide B on platelet-activating factor induced activation of rat polymorphonuclear leukocytes

AIM: To investigate the effect of ginkgolide B on PAF-induced adhesion, chemotaxis and degranulation of rat polymorphonuclear leukocytes (PMNs). METHODS: The adhesion of rat PMNs to rat synovial cells (RSC) was measured with MTT colorimetry. The chemotaxis of PMNs was quantified with Boyden chamber method. The degranulation of rat PMNs was evaluated by determining the activity of released beta-glucuronidase. RESULTS: In comparison with control, ginkgolide B at the concentration of 10 mumol.L-1 significantly inhibited the adhesion of PMNs to RSC by 71.74%. At the final concentration of 1-1,000 nmol.L-1, ginkgolide B dose-dependently inhibited the chemotaxis of PMNs stimulated with 10 nmol.L-1 platelet-activating factor (PAF), the IC50 was 4.84 nmol.L-1. At the final concentration of 0.01-10 mumol.L-1, ginkgolide B decreased the release of beta-glucuronidase in PMNs induced by 1 mumol.L-1 PAF in dose-dependent manner. The IC50 was 3.56 mumol.L-1. CONCLUSION: Ginkgolide B was found to significantly inhibit PAF-induced adhesion, chemotaxis and degranulation in rat polymorphonuclear leukocytes. These effects might be considered a part of the mechanisms underlying the antiinflammatory action of ginkgolide B.