Simpson L O, Aarons I, Howie J B
Br J Exp Pathol. 1979 Oct;60(5):493-8.
Thiamphenicol at the rate of 50 mg/kg/day given to female NZBxOUW F1 hybrid mice from weaning and continuing throughout life resulted in a considerable extension of lifespan, although this was less than in mice given the same drug dosage from first antinuclear antibody (ANA) positivity (Simpson, Aarons and Howie, 1979). Assessment of the changes in renal dysfunction and renal histology shows that thiamphenicol treatment did not prevent the development of immune complex glomerulonephritis although the rate of progression of the disease was slower than in untreated controls. Thiamphenicol failed to influence greatly the progressive anaemia which develops in these mice or to alter the pattern of ANA production. Although azotaemia developed in treated mice it was a terminal event. It was concluded that the action of thiamphenicol was to depress but not prevent immune complex formation possibly by impairing immunoglobulin formation although why immunofluorescent ANA formation remained unaffected is not understood.
从断奶开始并持续终生,以50毫克/千克/天的剂量给雌性新西兰黑×奥乌杂种小鼠施用甲砜霉素,可使寿命显著延长,尽管这一延长程度小于从首次出现抗核抗体(ANA)阳性起就给予相同药物剂量的小鼠(辛普森、阿伦斯和豪伊,1979年)。对肾功能障碍和肾脏组织学变化的评估表明,甲砜霉素治疗并不能预防免疫复合物性肾小球肾炎的发展,尽管疾病的进展速度比未治疗的对照组要慢。甲砜霉素对这些小鼠中逐渐发展的进行性贫血影响不大,也未改变ANA的产生模式。尽管接受治疗的小鼠出现了氮血症,但这是终末期事件。得出的结论是,甲砜霉素的作用是抑制而非预防免疫复合物的形成,可能是通过损害免疫球蛋白的形成来实现的,尽管为何免疫荧光ANA的形成未受影响尚不清楚。