摘要
目的 :研究高三尖杉酯碱对HL6 0细胞凋亡的影响及其机制。方法 :运用高三尖杉酯碱作用HL6 0细胞后撤药实验筛选其诱导HL6 0细胞凋亡启动时相 ,流式细胞和免疫组化技术检测高三尖杉酯碱诱导HL6 0细胞凋亡启动时相凋亡信号分子Bcl - 2、Bax、Fas/FasL、caspase - 3、ERK2和p38的表达状况。结果 :在高三尖杉酯碱诱导HL6 0细胞凋亡启动时相 ,Bcl- 2表达降低 ,Bax表达增高 ,Bcl - 2 /Bax比值降低 ,ERK2表达减低 ,p38表达增加 ,cas pase- 3表达增加 ,Fas/FasL分子的表达无显著变化。结论 :Bcl- 2、Bax、MAPK途径和caspase - 3参与高三尖杉酯碱启动HL6
AIM: To study the signal transduction pathway of apoptosis initiation induced by homoharringtonine in HL-60 cells. METHODS: After establishing the model of apoptosis initiation induced by homoharringtonine in HL-60 cells, at the point of apoptosis initiation, molecular caspase-3, Bcl-2, Bax and Fas/FasL were measured with flow cytometry and transmission electron microscope. ERK2 and P38 expression in HL-60 cells were detected by using immunohistochemistry. RESULTS: The model of apoptosis initiation induced by homoharringtonine was established in HL-60 cells. At the point of apoptosis initiation, upregulation of caspase-3 and decrease in Bcl-2/Bax were observed. However, the expression of Fas/FasL did not significantly change. ERK2 expression decreased and P38 expression increased. CONCLUSIONS: Caspase-3, Bcl-2, Bax and mitogen activated protein kinase pathways were involved in signal transduction of apoptosis initiation induced by homoharringtonine in HL-60 cells. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第7期1183-1186,共4页
Chinese Journal of Pathophysiology
