Yamashita W, Ito Y, Weiss M A, Ooi B S, Pollak V E
Department of Internal Medicine, University of Cincinnati College of Medicine, Ohio 45267-0585.
Prostaglandins Leukot Essent Fatty Acids. 1988 Dec;34(3):161-6. doi: 10.1016/0952-3278(88)90140-8.
To determine if the induction of immune-mediated glomerular injury influences the formation of glomerular cyclooxygenase products, we measured thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and prostaglandin E2 (PGE2) production by isolated glomeruli of rabbits induced with acute serum sickness nephritis by the administration of bovine serum ablumin (BSA). Animals were randomly assigned to one of three experimental groups: animals injected with BSA (BSA group; n = 11); animals injected with normal saline (control group; n = 11); and animals injected with BSA which were treated with the thromboxane synthetase inhibitor, OKY-046 (BSA + OKY-046; n = 6). Animals in the BSA and BSA + OKY groups developed severe proteinuria and glomerular histologic lesions of nephritis. No differences in proteinuria, serum creatinine and severity of histologic nephritis were observed between the two groups. Examination of glomerular eicosanoid production at the end of the experiment showed a marked reduction of glomerular PGE2 and 6-keto-PGF1 alpha production with a smaller reduction of glomerular TXB2 production in the BSA group. In the BSA + OKY-046 group, the production of TXB2 was significantly less than that in the BSA group; despite this, no effect on proteinuria could be discerned.
为了确定免疫介导的肾小球损伤的诱导是否会影响肾小球环氧化酶产物的形成，我们通过给予牛血清白蛋白（BSA）诱导兔急性血清病肾炎，测量了分离的兔肾小球中血栓素B2（TXB2）、6-酮-前列腺素F1α（6-酮-PGF1α）和前列腺素E2（PGE2）的产生。动物被随机分为三个实验组之一：注射BSA的动物（BSA组；n = 11）；注射生理盐水的动物（对照组；n = 11）；以及注射BSA并用血栓素合成酶抑制剂OKY-046治疗的动物（BSA + OKY-046组；n = 6）。BSA组和BSA + OKY组的动物出现了严重的蛋白尿和肾小球肾炎组织学病变。两组之间在蛋白尿、血清肌酐和组织学肾炎严重程度方面未观察到差异。实验结束时对肾小球类花生酸产生的检测显示，BSA组肾小球PGE2和6-酮-PGF1α的产生明显减少，而肾小球TXB2的产生减少幅度较小。在BSA + OKY-046组中，TXB2的产生明显低于BSA组；尽管如此，未发现对蛋白尿有影响。
