Hänsch G M, Betz M, Günther J, Rother K O, Sterzel B
Institute of Immunology, University of Heidelberg, FRG.
Int Arch Allergy Appl Immunol. 1988;85(1):87-93. doi: 10.1159/000234479.
Incubation of cultured rat glomerular epithelial cells (GEC) with sublytic amounts of the purified complement components C5b6, C7, C8 and C9 greatly stimulated the release of the prostanoids prostaglandin E (PGE) and thromboxane B2. Incubation of GEC with C5b-8 was also stimulatory, whereas omission of C7 abolished the enhanced prostanoid production. These effects were dose-dependent. The increased release of PGE was biphasic with peaks at 5 min and 24 h of incubation. The second peak could be prevented by treatment with cycloheximide, suggesting its dependence on protein synthesis. The observations on cultured GEC provide evidence that terminal complement components alter the metabolism of glomerular cells, resulting in increased production of prostanoids. The results are consistent with the concept that deposition of nonlytic amounts of complement in the glomerular capillary wall may affect the GEC in vivo and may indirectly contribute to abnormalities of the glomerular filter as it is seen in glomerular disease.
用亚溶解量的纯化补体成分C5b6、C7、C8和C9孵育培养的大鼠肾小球上皮细胞（GEC），可极大地刺激前列腺素E（PGE）和血栓素B2等类前列腺素的释放。用C5b-8孵育GEC也具有刺激作用，而省略C7则消除了类前列腺素生成的增强。这些效应呈剂量依赖性。PGE释放的增加是双相的，在孵育5分钟和24小时时出现峰值。第二个峰值可通过用环己酰亚胺处理来预防，这表明其依赖于蛋白质合成。对培养的GEC的观察提供了证据，表明补体末端成分改变了肾小球细胞的代谢，导致类前列腺素生成增加。这些结果与以下概念一致，即非溶解量的补体在肾小球毛细血管壁中的沉积可能在体内影响GEC，并可能间接导致肾小球滤过异常，正如在肾小球疾病中所见到的那样。
