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目的考察银杏内酯B(ginkgolide B,BN52021)对血小板活化因子(PAF)引起的小鼠腹腔巨噬细胞趋化反应和丝状肌动蛋白(F-actin)聚合作用的影响。方法Boyden小室法检测化合物对巨噬细胞趋化的影响;流式细胞术检测特异性标记的巨噬细胞中F-actin的变化。结果PAF可显著刺激小鼠腹腔巨噬细胞产生趋化效应,PAF受体拮抗剂BN52021(0.01 nmol.L-1~0.1μmol.L-1)可明显抑制该作用。此外,在含钙缓冲液中,BN52021可显著抑制PAF引起的丝状肌动蛋白聚合。结论BN52021可能通过抑制丝状肌动蛋白的聚合作用,从而抑制PAF引起的巨噬细胞趋化,并且这种作用是钙依赖性的。表明BN52021的抗炎作用途径之一是抑制PAF诱导的趋化作用。
Objective To investigate the effect of ginkgolide B (BN52021) on platelet activation factor (PAF)-induced chemotaxis of mouse peritoneal macrophages and the polymerization of filamentous actin (F-actin). Methods Boyden chamber method was used to detect the effect of compounds on macrophage chemotaxis. Flow cytometry was used to detect the changes of F-actin in specific labeled macrophages. Results PAF significantly stimulated the chemotaxis of mouse peritoneal macrophages. PAF receptor antagonist BN52021 (0.01 nmol.L-1~0.1 μmol.L-1) significantly inhibited this effect. In addition, BN52021 significantly inhibited PAF-induced filamentous actin polymerization in calcium-containing buffers. Conclusion BN52021 may inhibit the PAF-induced macrophage chemotaxis by inhibiting the polymerization of filamentous actin, and this effect is calcium-dependent. One of the anti-inflammatory effects of BN52021 is shown to inhibit PAF-induced chemotaxis.