OBJECTIVE: To study the influence of nitric oxide (NO) in rats with anemia in chronic disease (ACD) and the effect of NO on the expression of transferrin receptor (TfR) in bone marrows and to provide experimental evidence for the prevention and treatment of ACD. METHODS: The conventional animal model of rheumatoid arthritic (RA) was established by injection of Freund's complete adjuvant. On the basis of this model, we injected Freund's complete adjuvant repeatedly to establish the ACD model. The rats were randomly assigned into three groups (Group A: control group; Group B: inflammatory group; Group C: inflammatory + NO inhibitory agent group). The histopathological changes of the toe joints of the rats were observed and the contents of NO, Hb and nitric oxide synthetase (NOS), and the expression of TfR were measured in the three groups. RESULTS: In Group B, the contents of NO and NOS in the serum were higher than those in Group A; TfR expression in bone marrow cells was lower than that in Group A, and anemia was more severe than that in Group A. After administrating NOS inhibitory agent (L-NAME), anemia was improved; the contents of NO and NOS remarkably decreased compared with those in Group B, but were still higher than those in Group A; TfR in bone marrow cells obviously increased compared with that in Group B, but was still lower than that in Group A. CONCLUSIONS: NO may play an important role in the pathogenesis of ACD and regulation of TfR on ACD, thereby providing experimental evidence for further study of the pathogenesis of ACD. It is helpful in hindering the development of anemia by reducing the NO level as early as possible, and is a new way of treating ACD."/>
NO对慢性病贫血大鼠转铁蛋白受体表达的影响(英文)
Abstract：OBJECTIVE: To study the influence of nitric oxide (NO) in rats with anemia in chronic disease (ACD) and the effect of NO on the expression of transferrin receptor (TfR) in bone marrows and to provide experimental evidence for the prevention and treatment of ACD. METHODS: The conventional animal model of rheumatoid arthritic (RA) was established by injection of Freund's complete adjuvant. On the basis of this model, we injected Freund's complete adjuvant repeatedly to establish the ACD model. The rats were randomly assigned into three groups (Group A: control group; Group B: inflammatory group; Group C: inflammatory + NO inhibitory agent group). The histopathological changes of the toe joints of the rats were observed and the contents of NO, Hb and nitric oxide synthetase (NOS), and the expression of TfR were measured in the three groups. RESULTS: In Group B, the contents of NO and NOS in the serum were higher than those in Group A; TfR expression in bone marrow cells was lower than that in Group A, and anemia was more severe than that in Group A. After administrating NOS inhibitory agent (L-NAME), anemia was improved; the contents of NO and NOS remarkably decreased compared with those in Group B, but were still higher than those in Group A; TfR in bone marrow cells obviously increased compared with that in Group B, but was still lower than that in Group A. CONCLUSIONS: NO may play an important role in the pathogenesis of ACD and regulation of TfR on ACD, thereby providing experimental evidence for further study of the pathogenesis of ACD. It is helpful in hindering the development of anemia by reducing the NO level as early as possible, and is a new way of treating ACD.
WANG Qiang,LIAO Qing-Kui,DONG Wei. Effect of Nitric Oxide on the Expression of Transferrin Receptor in Rats with Anemia in Chronic Disease[J]. CJCP, 2003, 5(2): 90-94.
