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目的探讨IFN-γ、TNF-α在免疫介导的再生障碍性贫血小鼠中的致病作用。方法根据文献方法建立免疫介导的再生障碍性贫血小鼠模型,设立正常对照组,于实验第13天,全部处死小鼠,检测外周血红细胞、白细胞、血红蛋白、血小板及血清中的IFN-γ、TNF-α含量,计数骨髓有核细胞。结果模型组小鼠的白细胞、红细胞、血红蛋白、血小板及骨髓有核细胞数均显著下降,与正常对照组比较差异有统计学意义(P<0.01);符合再生障碍性贫血的表现。血清中的IFN-γ含量与正常对照组比较明显升高,两者差异有统计学意义(P<0.01),TNF-α含量比正常对照组略增高,但差异无统计学意义(P>0.05)。结论本实验条件下所建立的免疫介导的再生障碍性贫血小鼠模型是成功的,IFN-γ含量的升高在免疫介导的再生障碍性贫血模型小鼠中具有肯定的致病作用,而TNF-α的含量在本实验条件下建立的再障模型小鼠血清中增高不明显。
Objective To investigate the pathogenicity of IFN-γ and TNF-α in immune-mediated aplastic anemia mice. Methods According to the literature method, immune-mediated aplastic anemia mouse model was established and normal control group was set up. All mice were sacrificed on the 13th day of experiment to detect IFN-γ in peripheral blood red blood cells, white blood cells, hemoglobin, platelets and serum , TNF-α content, count bone marrow nucleated cells. Results The numbers of leukocytes, erythrocytes, hemoglobin, platelets and bone marrow nucleated cells in model group were significantly decreased compared with those in normal control group (P <0.01), which met the performance of aplastic anemia. The level of IFN-γ in serum was significantly higher than that of the normal control group (P <0.01), and the content of TNF-α was slightly higher than that of the normal control group (P> 0.05 ). Conclusions The immune-mediated aplastic anemia mouse model established in this experiment was successful. Elevated IFN-γ level had a positive pathogenicity in immune-mediated aplastic anemia mice, However, the level of TNF-α in the aplastic anemia model mice established in this experiment was not significantly increased in serum.