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为探讨类风湿性关节炎 (RA)伴慢性疾病性贫血 (ACD)血清中IFN -γ和Epo变化 ,及其发病中作用的可能机制。采用ELISA法检测RA患者血清中IFN -γ及RA伴ACD患者的Epo变化。并以人肝癌细胞株HepG2 为模型 ,观察IFN -γ对钴盐 (CoCl2 )诱导的Epo产生的影响。与正常对照组比较 ,RA及伴ACD者血清中IFN -γ显著增高 ,与血红蛋白浓度呈负相关。RA伴ACD者的Epo水平高于正常对照组 ,但低于同等贫血程度的单纯IDA组。IFN -γ能抑制钴盐 (CoCl2 )诱导HepG2 的Epo生成。说明RA伴ACD者体内Epo相对不足 ,IFN -γ可能通过抑制Epo的生成导致红细胞生成减少而介导RA的ACD发病
To investigate the changes of IFN-γ and Epo in the serum of rheumatoid arthritis (RA) with chronic disease-associated anemia (ACD) and its possible mechanism. The serum levels of IFN-γ and RA with ACD in RA patients were detected by ELISA. The effect of IFN-γ on ECl2 production induced by CoCl2 was observed by using human hepatocellular carcinoma cell line HepG2 as a model. Compared with the normal control group, the levels of IFN-γ in serum of RA and ACD patients were significantly increased, and negatively correlated with hemoglobin concentration. The Epo level of RA with ACD was higher than that of normal control group, but lower than that of IDA group with the same degree of anemia. IFN-γ inhibits cobalt chloride (CoCl2) -induced HepG2 Epo production. These results suggest that Epo is relatively deficient in RA patients with ACD. IFN-γ may mediate the pathogenesis of RA in ACD by inhibiting the production of Epo, leading to the decrease of erythropoietin