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目的：探讨血小板活化因子受体拮抗剂对实验性肾病综合征的疗效及机制。方法：实验大鼠均复制成阿霉素（ＡＤＲ）肾病模型，分为２组：ＡＤＲ肾病组和ＡＤＲ肾病＋血小板活化因子（ＰＡＦ）受体拮抗剂（ＢＮ５２０２１）组。结果： ＡＤＲ肾病＋ＢＮ５２０２１组大鼠各期尿蛋白量、血清总蛋白下降幅度、血清胆固醇上升幅度均显著低于ＡＤＲ肾病组（Ｐ＜０．０５），第２１ｄ时血清肌酐含量显著低于ＡＤＲ肾病组（Ｐ＜０．０５）；电镜下肾组织病理改变显著轻于ＡＤＲ肾病组。 ＡＤＲ肾病组中，肾皮质 ＰＡＦ最大产量在１４ ｄ（先于最大蛋白尿量），而肿瘤坏死因子（ＴＮＦα）最大含量在２１ｄ，而且，ＡＤＲ肾病＋ＢＮ５２０２１组肾皮质内 ＰＡＦ、ＴＮＦα含量显著低于ＡＤＲ肾病组。结论：ＰＡＦ可能直接或间接通过刺激肾小球团有细胞（肾小球系膜细胞、上皮细胞等）产生ＴＭＦ导致肾小球损伤，ＰＡＦ拮抗剂可能通过抑制肾皮质内ＰＡＦ、ＴＮＦα合成，而减轻肾小球损伤。
Objective: To investigate the therapeutic effect and mechanism of platelet-activating factor receptor antagonist on experimental nephrotic syndrome. METHODS: All experimental rats were duplicated into adriamycin (ADR) nephropathy model and divided into two groups: ADR nephropathy group and ADR nephropathy + platelet activating factor (PAF) receptor antagonist (BN52021) group. Results: The levels of urinary protein, serum total protein and serum cholesterol in ADR nephropathy + BN52021 group were significantly lower than those in ADR nephropathy group (P <0.05), serum creatinine was significantly lower than that in ADR nephropathy Group (P <0.05). The pathological changes of renal tissue under electron microscope were significantly lighter than those of ADR nephropathy group. In ADR nephropathy group, the maximal production of PAF in renal cortex was 14 days (before maximal proteinuria) and the maximum content of tumor necrosis factor (TNFα) was 21 days. Moreover, the content of PAF and TNFα in renal cortex of ADR nephropathy + BN52021 group was significantly lower than that of ADR nephropathy group. Conclusion: PAF may induce glomerular damage directly or indirectly by stimulating the production of TMF in glomerular cells (mesangial cells, epithelial cells, etc.). PAF antagonists may inhibit the synthesis of PAF and TNFα in renal cortex Reduce glomerular injury.