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目的 探讨一氧化氮(NO)在慢性病贫血(ACD)发病中的作用及对骨髓血细胞转铁蛋白受体(TfR)的影响,为ACD的防治提供实验依据。方法用福氏完全佐剂建立传统的类风湿性关节炎大鼠动物模型,在此基础上通过反复注射福氏完全佐剂,建立ACD大鼠动物模型。利用此模型观察对照组、炎症组及炎症十一氧化氮合酶(NOS)抑制剂组的NO浓度的改变、贫血的程度及与TfR的关系。结果 炎症组NO、NOS浓度显著高于对照组,贫血明显,TfR表达强度低于对照组,差异有显著性(P<0.01);用NOS抑制剂后,NO和NOS水平低于炎症组但仍高于对照组,贫血改善,TfR介于炎症组与对照组之间,差异有显著性(P<0.01)。结论NO参与了ACD的发病及ACD时TfR的调节,为从NO对TfR影响角度进一步认识ACD的发病机制提供了实验依据;及早降低NO水平,有利于阻止贫血的发展,为ACD的治疗提供一条新途径。
Objective To investigate the role of nitric oxide (NO) in the pathogenesis of chronic disease-related anemia (ACD) and its effect on the expression of transferrin receptor (TfR) in bone marrow blood and provide experimental evidence for the prevention and treatment of ACD. Methods The traditional animal models of rheumatoid arthritis were established by Freund’s complete adjuvant. On the basis of repeated adjuvant injection of Freund’s adjuvant, animal models of ACD rats were established. The model was used to observe the change of NO concentration, the degree of anemia and the relationship with TfR in the control group, inflammatory group and inflammatory nitric oxide synthase (NOS) inhibitor group. Results The levels of NO and NOS in the inflammation group were significantly higher than those in the control group, the anemia was obvious and the expression of TfR was lower than that in the control group (P <0.01). The levels of NO and NOS in the inflammation group were lower than those in the control group Higher than the control group, anemia improved, TfR between the inflammation group and the control group, the difference was significant (P <0.01). Conclusions NO participates in the pathogenesis of ACD and the regulation of TfR in ACD. It provides an experimental basis for further understanding the pathogenesis of ACD from the perspective of the influence of NO on TfR. It is helpful to prevent the development of anemia by reducing the NO level as early as possible, providing a New way.