W Miyazaki, T Izawa, Y Nakano, M Shinohara, K Hing, T Kinoshita, K Inoue
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引用次数: 29
摘要
在豚鼠或大鼠体内注射K-76单羧酸(K-76 COOH)后,补体及其部分成分(尤其是C5)的溶血活性迅速降低。K-76 COOH对豚鼠和小鼠的Forssman休克和豚鼠的异源被动皮肤过敏反应有抑制作用。它还减少了肾毒性肾炎大鼠尿液中蛋白质的排泄量,并大大延长了(NZB X NZW) F1雌性小鼠自发性系统性红斑狼疮样疾病的存活时间。经K-76 COOH处理的小鼠肾小球即使在1岁时也几乎保持正常的组织学外观。K-76 COOH处理的小鼠对大肠杆菌、金黄色葡萄球菌或肺炎链球菌的感染变得不那么敏感,可能是由于抑制因子i而增强了吞噬作用,K-76 COOH对小鼠的延迟型接触性皮肤反应或豚鼠的实验性过敏性脑炎没有任何显著影响。
Effects of K-76 monocarboxylic acid, an anticomplementary agent, on various in vivo immunological reactions and on experimental glomerulonephritis.
K-76 monocarboxylic acid (K-76 COOH) caused rapid reduction in hemolytic activities of complement and some of its components, especially C5, when injected into guinea pigs or rats. K-76 COOH suppressed Forssman shock in guinea pigs and mice and heterologous passive cutaneous anaphylaxis in guinea pigs. It also reduced the amount of protein excreted in the urine of rats with nephrotoxic nephritis and greatly prolonged the survival of (NZB X NZW) F1 female mice with a spontaneous systemic lupus erythematosus-like disease. The glomeruli of mice treated with K-76 COOH retained almost the normal histological appearance even at 1 year of age. K-76 COOH-treated mice became less sensitive to the infection of Escherichia coli, staphylococcus aureus, or Streptococcus pneumoniae, probably by enhancement of phagocytosis due to inhibition of factor I. K-76 COOH did not have any significant effect on a delayed-type contact skin reaction in mice, or on experimental allergic encephalitis in guinea pigs.