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为了研究成人急性髓性白血病(acute myeloid leukemia,AML)骨髓细胞凋亡促进分子---PDCD5的表达,以探讨PDCD5在AML发病机制中的作用,利用21种不同荧光标记的单克隆抗体标记骨髓细胞,通过流式细胞术检测AML病人及正常人骨髓不同群细胞的胞内PDCD5的表达。部分标本进行蛋白印迹实验检测AML病人及正常人骨髓细胞内PDCD5的表达。结果表明:36例未治AML病人骨髓总的有核细胞内PDCD5平均荧光强度明显低于30例正常人组,分别为3059±1392:7432±1261(P<0.01),其中未治AML病人骨髓粒细胞、单核细胞、幼稚细胞及淋巴细胞内PDCD5平均荧光强度均低于相应的正常人组骨髓细胞,分别为3939±2121:8367±1045;3156±1635:5917±2329;2824±1592:3998±2106;1474±816:3355±2042(P值均小于0.01)。部分标本进行蛋白印迹检测的结果也显示AML病人骨髓细胞内PDCD5的表达低于正常人。结论:未治AML病人骨髓总有核细胞的PDCD5表达低于正常人,未治AML病人骨髓粒细胞、单核细胞、幼稚细胞及淋巴细胞内PDCD5表达均低于正常人组骨髓细胞。PDCD5的异常表达可能在AML的病理机制中起到一定的作用。
In order to study the expression of PDCD5, an apoptosis-promoting molecule of adult myeloid leukemia (AML), in order to investigate the role of PDCD5 in the pathogenesis of AML, 21 different fluorescently labeled monoclonal antibodies were used to label bone marrow Cells were detected by flow cytometry AML patients and normal human bone marrow cells of different groups of intracellular PDCD5 expression. In some samples, Western blotting was used to detect the expression of PDCD5 in bone marrow cells of AML patients and normal human. The results showed that the mean fluorescence intensity of PDCD5 in the total nucleated cells of 36 untreated AML patients was significantly lower than that of 30 healthy controls (3059 ± 1392: 7432 ± 1261, P <0.01) The mean fluorescence intensity of PDCD5 in granulocytes, monocytes, naive cells and lymphocytes were lower than that of corresponding normal human bone marrow cells (3939 ± 2121: 8367 ± 1045; 3156 ± 1635: 5917 ± 2329; 2824 ± 1592: 3998 ± 2106; 1474 ± 816: 3355 ± 2042 (all P values less than 0.01). The results of Western blotting on some specimens also showed that the expression of PDCD5 in bone marrow cells of AML patients was lower than that in normal people. Conclusion: The expression of PDCD5 in bone marrow mononuclear cells of patients with untreated AML is lower than that in normal controls. The expression of PDCD5 in bone marrow mononuclear cells, immature cells and lymphocytes in untreated AML patients is lower than that in normal people. Aberrant expression of PDCD5 may play a role in the pathogenesis of AML.