血小板活化因子受体拮抗剂干扰实验性肾炎的疗效观察及机理探讨

实验大鼠均制成加速型抗肾小球基膜（GBM）肾炎模型，分为三组：模型组、血小板活化因子（PAF）受体拮抗剂BN－52021组和血栓素A2（TXA2）合成酶抑制剂UK－38485组，结果BN－52021组大鼠各期尿蛋白量较模型组显著减少（P＜0．01），第21天时血清肌酐、肾皮质内TXB2含量较模型组显著降低（P＜0．01）；光镜和电镜下肾组织病理改变明显较模型组为轻；UK-8485组尿蛋白量也倾向于较模型组减少，担无统计学意义．第21天时血清肌酐、肾皮质内TXB2含量也较模型组显著降低（P＜0．01）．本实验表明，PAF受体拮抗剂干扰该大鼠肾炎有效，其有效机理可能部分是通过减少肾皮质TXA2合成而介导的。

Effects of PAF receptor antagonist on the rat model of glomerulonephritis

Rat model of accelerated anti-GBM glomerulonephritis was used in the present study. Rats were divided into three groups:the control group,PAF receptor antagonist BN 52021 group and selective TXA, syn-thetase inhibitor UK-38485 group. The re-sults showed: In the BN 52021 group, the proteinuria were significantly decreased. At the 21th day,Scr,the amount of TXB2 in the renal cortex were significantly reduced. By light and electron microscopy,the renal his-tological changes were significantly more minor than that in the control group. In the UK-38485 group,the proteinuria trended to be decreased when compared with that in the control group. At the 21th day, Scr, the amounts of TXB2 in the renal cortex were significantly reduced. The renal histological changes were similar to that in the BN-52021 group. These suggest that PAF re-ceptor antagonist is effective in interference v-ith the rat model of glomerulonephritis and some pathophysiologic consequences of PAF release are mediated by the intrarenal formation of TXA2.