摘要
目的探讨一氧化氮(NO)在慢性病贫血(ACD)发病中的作用及对肝脏顺乌头酸酶(aconitase)活性的影响,为ACD的防治提供实验依据。方法通过反复注射福氏完全佐剂在传统的类风湿性关节炎动物模型基础上建立了ACD大鼠动物模型。由于铁调节蛋白1(IRP-1)与aconitase有高度的同源性,aconitase又是NO主要靶酶,故利用此模型观察了不同处理组NO浓度的改变与贫血及肝脏aconitase活性的关系。结果炎症组NO浓度显著增高,贫血明显,aconitase活性降低,用一氧化氮合酶(NOS)抑制剂后,NO水平降低,贫血改善,aconitase活性介于炎症组与正常对照组之间。统计学处理有显著性差异P<0.01。结论NO参与了ACD的发病,为从NO角度进一步认识ACD的发病机制提供了实验依据。为ACD的治疗提供了一条新途径。
Objective To explore the effect of nitric oxide （NO） on the pathogenesis and regulation of aconitase in anemia of chronic disease （ACD） ; to provide experimental evidence for prevention and treatment of ACD. Methods The traditional animal model of rheumatoid arthritic（RA） was established by injecting Freund＇ s complete adjuvant into rats one time. On the basis of the model we injected this adjuvant twice so that anemia was induced. The different groups were treated with endogenous NO inhibitory agent L-NAME or NS, measured nitric oxide in the serum and livers and the aconitase of the livers of three groups treated with three different ways. Results The different degree anemia was induced; in the ACD group NO in the serum and livers increased; the aconitase activity in the livers decreased; anemia was remarkable. After taking L-NAME, anemia was improved; NO decreased and the aconitase activity in the livers elevated. On-way analysis of variance between them was significant difference P 〈 0. 01. Conclusion NO plays an important role in pathogenesis of ACD, which provides experimental evidence for the pathogenesis of ACD. Decreased NO levels as early as possible blocks the development of anemia. It shows one of the new ways to treat ACD.
出处
《中国小儿血液与肿瘤杂志》
CAS
2007年第6期257-259,共3页
Journal of China Pediatric Blood and Cancer
