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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。
Objective To investigate the mechanism of apoptosis induced by homoharringtonine in HL-60 leukemia cells. Methods Cell morphology, DNA agarose gel electrophoresis, immunohistochemistry, Northern hybridization and other methods were used. RESULTS: The HL-60 leukemia cells exhibited typical apoptotic characteristics under the action of homoharringtonine. Morphology showed nuclear lysis, chromatin aggregation, nuclear fragmentation, cytoplasm condensation, vacuolization, and agarose electrophoresis. A typical DNA ladder appears. Immunohistochemical detection of anti-apoptotic protein Bcl-2 significantly decreased after treatment, pro-apoptotic protein Bax no significant changes, Northern hybridization found that Bcl-2mR-NA expression was not significantly reduced after treatment. Conclusion One of the mechanisms of apoptosis induced by homoharringtonine is to decrease the level of anti-apoptotic protein Bcl-2. The reason for the decrease of Bcl-2 protein may be that homoharringtonine promotes the degradation of Bcl-2 protein.