论文部分内容阅读
目的 :探讨血小板活化因子 (PAF)对肾小球系膜细胞 (GMC)合成前列腺素E2 (PGE2 )的影响及其意义。 方法 :测定PAF刺激对GMC合成PGE2 的影响。 结果 :PAF刺激GMC显著增加PGE2 的合成并呈剂量依赖性。 10 -5mol/LPAF在 5min内即刺激GMC合成PGE2 显著增加。刺激PGE2 合成的PAF阈值为 10 10mol/L ,刺激半量和最大量PGE2 合成的PAF浓度分别约为 10 -8mol/L和 10 -7mol/L。溶PAF无刺激GMC合成PGE2 作用。PAF受体拮抗剂BN5 2 0 2 1能抑制PAF刺激GMC合成PGE2 。PGE2 对肾小球功能有保护作用。 结论 :PAF介导肾小球肾炎发病中的作用 ,能由其诱导PGE2 合成增加所中和
Objective: To investigate the effect of platelet activating factor (PAF) on the synthesis of prostaglandin E2 (PGE2) in glomerular mesangial cells (GMC) and its significance. Methods: To determine the effect of PAF stimulation on the synthesis of PGE2 by GMC. Results: PAF stimulation of GMC significantly increased the synthesis of PGE2 in a dose-dependent manner. 10 -5mol / LPAF stimulated GMC synthesis PGE2 significantly increased within 5min. The PAF threshold for stimulating PGE2 synthesis was 10 10 mol / L, and PAF concentrations for the stimulated half and maximal PGE2 were about 10 -8 mol / L and 10 -7 mol / L, respectively. PAF did not stimulate GMC synthesis of PGE2 role. PAF receptor antagonist BN5 2 0 2 1 can inhibit PAF stimulating GMC synthesis of PGE2. PGE2 has a protective effect on glomerular function. Conclusions: The role of PAF in the pathogenesis of glomerulonephritis can be induced by its increased PGE2 synthesis