【摘要】 目的探讨高三尖杉酯碱诱导HL-60白血病细胞凋亡的机制。方法应用细胞形态学、DNA琼脂糖凝胶电泳、免疫组织化学、Northern杂交等方法。结果HL-60白血病细胞在高三尖杉酯碱的作用下，出现典型的凋亡特征，形态学表现出细胞核裂解，染色质聚集，核碎裂，胞浆浓缩，有空泡形成，琼脂糖电泳出现典型DNA梯带。免疫组化检测抗凋亡蛋白Bcl-2在用药后明显下降，促凋亡蛋白Bax无明显变化，Northern杂交发现Bcl-2mR-NA在用药后表达无明显降低。结论高三尖杉酯碱诱导凋亡的机制之一是降低抗凋亡蛋白Bcl-2水平,Bcl-2蛋白降低的原因可能是高三尖杉酯碱促进Bcl-2蛋白降解。更多还原

【Abstract】 To investigate the mechanisms of homobarringtonine inducing apoptoris in HL-60 leukemia cello.Methods Cell morphollogy. DNA agarose gel electrophoresis.immunohistochemistry and Northen hlot were performed.Results HL-60 leukemia cells treated with homoharringtonine underwent apoptosis. Apoptosis cells demonstrated compaction and segregation of the nuclear chromatin. condensation and vacuolus of the cytoplasm. Nuclear DNA of apoptosis cells display ladder bands charateristic of internucleosomal DNA fragmenlation. Protein expression of Bcl-2. inhibitor of apoptosis. was obviously decreased.while that of Bax, inducer of apoptosis had no changes. MRNA expression of Bcl-2 examined by Northern blot had no changes.Conclusion The mechanism of homoharringtonine inducing apoptosis in HL-60 cells is decreasing Bcl-2 protein expression. The altered expression of Bcl-2 may be caused by degradation of Bcl-2 protein.更多还原