Gabrielsen A E, Olsen C T
Clin Exp Immunol. 1979 Jan;35(1):33-5.
Dactinomycin treatment a of group of (NZB X NZW)F1 hybrid female mice was delayed until the age of 6-6 1/2 months, by which time the immune complex disease was well established. Three animals of the original twenty-eight had already died, ten had heavy proteinuria and a few were oedematous. The dactinomycin dose was 3.5 microgram per day, which was suspended when significant weight loss occurred. Twelve of the thirteen experimental mice were alive at 12 months of age, eleven at 15 months, but only eight by 20 months, whereas all twelve control animals had died by the age of 11 months. These results and the supporting data on body weight and renal function indicate that dactinomycin can at least arrest the disease process and may improve it. The mechanism is not known, but it may be the result of a reduced availability of DNA or an alteration in its properties following combination with dactinomycin.
对一组（新西兰黑鼠×新西兰白鼠）F1杂交雌性小鼠使用放线菌素D进行治疗的时间推迟至6至6个半月龄，此时免疫复合物疾病已充分发展。最初的28只动物中有3只已经死亡，10只出现严重蛋白尿，还有几只出现水肿。放线菌素D的剂量为每天3.5微克，当出现明显体重减轻时暂停给药。13只实验小鼠中有12只在12个月龄时存活，11只在15个月龄时存活，但到20个月龄时只有8只存活，而所有12只对照动物在11个月龄时均已死亡。这些结果以及关于体重和肾功能的支持数据表明，放线菌素D至少可以阻止疾病进程，并且可能改善病情。其机制尚不清楚，但可能是由于与放线菌素D结合后DNA的可用性降低或其性质发生改变所致。
