Effect Of Nitric Oxide On Pathogenesis And Regulation Of Iron Metabolism Of ACD Rat:an Preliminary Experimental Study

Objective 1 To establish a rat model of anemia of chronic disease (ACD) and lay a foundation for further studying pathogenesis of ACD; 2 To explore the effect of nitric oxide (NO) on the pathogenesis and regulation of iron metabolism of ACD; 3 To provide experimental evidence for prevetion and treatment of ACD. Methods 1 The tranditional animal model of rheumatoid arthritic(RA) was eatablished by injecting Freund s complete adjuvant into rats only time. On the basis of the model we injected Freund s complete adjuvant twice again so that anemia was induced; 2 The different groups were treated with endogenous NO inhibitory angent L-NAME or NS; 3 Observe the histopathlogical change of the toe joints of rats;4.Measure the iron, total iron binding capacity(TIBC), transferrin saturation (TS), ferrin(Fn),nitric oxide(NO), nitric oxide synthase(NOS) in the serum and Fn in the erythrocytes of rats treatde with three different ways; 5 Detect the tranferrin receptor(TfR)and iron in the bone marrow cells of three groups; 6 Examine theaconitase, NO,iron in the rat livers of three groups. Results 1 Different degree anemia was induced by injecting the Freund s complete adjuvant into adjuvant arthritis rats; 2 in the ACD group NO,NOS in the serum increased; the iron,TIBC, TS in the serum and Fn in the erythrocytes decreased;Fn in the serum and iron in the livers increased. These changes were consistent with the characteristics of iron metablism disorder in ACD.meanwhile the aconitase activity in the livers decreased. After taking L-NAME, anemia was improved; NO ,NOS decreased;iron, TS,TIBC in the serum increased ;iron in the livers and Fn in the serum decreased;TfR,iron in bone marrow increased;the aconitase activity in the liver elevated.On-way analysis of variance between them was significant difference P<0.01.Conclusion 1 By injecting Freund s complete adjuvant into rats times ,ACD animal model can be established; 2 NO plays an important role in pathogenesis of ACD and arthritis; 3 NO influence regulation of iron metabolism on ACD,which provides new experimental evidence for the pathogenesis of ACD ; 4 Decreased NO levels as early as possible benefits to block the development of anemia and damaged tissues. It offers the new experimental evidence for pathogenesis of ACD. It shows that one of the new ways to treat ACD is to explore and produce specific NO and INOS(inducible nitric oxide synthase) inhibitor angents.