检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
机构地区:[1]广州医学院附属广州市第二人民医院血液科,广东广州51010
出 处:《中国医师杂志》2000年第11期648-650,共3页Journal of Chinese Physician
摘 要:为探讨急性髓系白血病 (AML)原代细胞自分泌的粒细胞—巨噬细胞集落刺激因子 (GM -CSF)和重组人粒细胞—巨噬细胞集落刺激因子 (rhGM -CSF)对原代AML细胞凋亡的影响 ,应用放射免疫技术检测GM -CSF水平 ,DNA电泳检查梯状条带及流式细胞仪检测细胞凋亡率和Bcl- 2蛋白表达的阳性细胞率和相对荧光强度 (MFI)。结果在 5例原代AML细胞体外培养中 ,3例的培养上清液可检测到GM -CSF ,其自发细胞凋亡率比其余 2例明显减少 ;bcl- 2蛋白表达的MFI明显增强。阿糖胞苷 (Ara -C) 5μg/ml联合rhGM -CSF 5ng/ml作用AML细胞 2 4h ,细胞凋亡率比单独Ara -C组显著增加达 (56 4± 7 4 ) % (P <0 0 5)。说明有自分泌GM -CSF的AML细胞自发凋亡率低 ,其机制可能与GM -CSF提高bcl- 2蛋白表达有关 ;rhGM -CSF能够增强AraTo investigate the effects of granulocyte macrophage colony stimulating factor (GM-CSF) which was secreted from the fresh leukemic cells of patients with acute myeloid leukemia (AML) and recombinant human GM-CSF(rhGM-CSF) on the apoptosis of the primary incubative AML cells,the level of GM-CSF was measured by means of radioimmunoassay,the DNA ladder was detected by using DNA electrophoresis,and the percentage of apoptotic cells,percentage of expression and the mean fluorescence intensity(MFI) of bcl-2 were respectively assayed by means of flow cytomtric analysis.After the fresh leukemic cells from 5 cases were incubated for 24 hours,GM-CSF in 3 of 5 cases were seen,their percentage of apoptotic cells was less than the other 2 cases,and the MFI of bcl-2 in the 3 of 5 cases was obviously enhanced.After the fresh leukemic cells were treated with cytarabine (Ara-C) 5μg/ml in combination with rhGM-CSF 5μg/ml for 24 hours,the percentage of apoptotic cells was more than the cells treated with Ara-C alone and it upward to (56 4±7 4)%(p<0 05,n=5).It is suggested that the GM-CSF autosecreted by fresh AML cells could inhibit the spontaneous apoptosis in the cells and its mechanism may be related to the increase of bcl-2 expression.The rhGM-CSF can augment apoptosis of AML cells induced by Ara-C.
分 类 号:R733.710.2[医药卫生—肿瘤]
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.28