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| 高三尖杉酯碱对HL60细胞凋亡的影响及机制的研究 | |
| 引用本文： | 陈春燕,贾继辉,潘祥林,张琦,王涓冬,周亚滨. 高三尖杉酯碱对HL60细胞凋亡的影响及机制的研究[J]. 中国病理生理杂志, 2004, 20(7): 1183-1186 |
| 作者姓名： | 陈春燕 贾继辉 潘祥林 张琦 王涓冬 周亚滨 |
| 作者单位： | 1. 山东大学第二医院血液－肿瘤科, 山东 济南 250033; 2. 山东大学医学院微生物学教研室, 山东 济南 250012; 3. 山东大学实验畸形学教育部重点实验室, 山东 济南 250012 |
| 摘 要： | 目的:研究高三尖杉酯碱对HL60细胞凋亡的影响及其机制。方法:运用高三尖杉酯碱作用HL60细胞后撤药实验筛选其诱导HL60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HL60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HL60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,caspase-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HL60细胞凋亡的信号转导。 |
| 关 键 词： | 白血病 HL60细胞 细胞凋亡 信号转导 高三尖杉酯碱 |
| 文章编号： | 1000-4718(2004)07-1183-04 |
| 收稿时间： | 2004-01-12 |
| 修稿时间： | 2004-04-02 |
The mechanism of apoptosis induced by homoharringtonine in HL - 60 cells |
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| CHEN Chun-yan,JIA Ji-hui,PAN Xiang-lin,ZHANG Qi,WANG Juan-dong,ZHOU Ya-bin. The mechanism of apoptosis induced by homoharringtonine in HL - 60 cells[J]. Chinese Journal of Pathophysiology, 2004, 20(7): 1183-1186 | |
| Authors: | CHEN Chun-yan JIA Ji-hui PAN Xiang-lin ZHANG Qi WANG Juan-dong ZHOU Ya-bin |
| Affiliation: | 1. Department of Hematology and Oncology, The Second Hospital of Shandong University, Jinan 250033, China; 2. Department of Microbiology, School of Medicine, Ministry of Education, Shandong University, Jinan 250012, China; 3. The Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University, Jinan 250012, China |
| Abstract: | 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. [ |
| Keywords: | Leukemia HL-60 cells Apoptosis Signal transduction Homoharringtonine |
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