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二异丙基磷酰化二肽甲酯通过线粒体途径诱导K562细胞凋亡
刘峰 ; 蒋宇扬 ; 刘世英 ; 王凯 ; 曹健 ; 赵玉芬 ; LIU Feng ; JIANG Yu-Yang ; LIU Shi-Ying ; WANG Kai ; CAO Jian ; ZHAO Yu-Fen
2010-06-10 ; 2010-06-10
关键词磷酰肽甲酯 细胞凋亡 线粒体跨膜电位 活性氧 K562细胞 Phosphoryl peptide methyl ester Apoptosis Mitochondrial membrane pot ential (Δψm) Reactive oxygen species K562 cells R73-3
其他题名Inducement Effect of (DIPP-L-Trp)2-L-Lys-OCH3 on Apoptosis of K562 Cells Through Mitochondrial-dependent Pathway
中文摘要背景与目的:蛋白质和多肽的磷酰化在生命活动中具有重要的作用,研究发现部分磷酰化肽有抑制肿瘤细胞增殖的活性,但其具体机理还不清楚。本研究探讨二异丙基磷酰化二肽甲酯[(O,O鄄diisopropylphosphoryl鄄L鄄tryptophan)2鄄L鄄lysinemethylester,(DIPP鄄L鄄Trp)2鄄L鄄Lys鄄OCH3]诱导K562细胞凋亡的作用及其可能的机制。方法:AnnexinV鄄FITC和PI双染法检测(DIPP鄄L鄄Trp)2鄄L鄄Lys鄄OCH3诱导的K562细胞凋亡。以罗丹明123(Rhodamine123)及2蒺,7蒺鄄二氯荧光素乙二酯(2蒺,7蒺鄄dichlorofluoresceindiacetate,DCFH鄄DA)为细胞染色剂,采用流式细胞术检测以不同浓度(DIPP鄄L鄄Trp)2鄄L鄄Lys鄄OCH3处理后K562细胞线粒体膜电位(Δψm)和活性氧(reactiveoxygenspecies,ROS)的变化。结果:50μg/ml(DIPP鄄L鄄Trp)2鄄L鄄Lys鄄OCH3作用细胞24h,AnnexinV鄄FITC和PI双染检测表明,有61.9%的细胞出现早期凋亡现象。Rhodamine123染色发现93.6%的细胞线粒体膜电位强度下降,随着化合物作用时间的延长,Δψm下降的细胞逐步增加到95.8%,同时DCFH鄄DA处理24h后97.6%的细胞ROS生成下降,ROS下降的细胞比例从18.1%增加到97.6%。结论:(DIPP鄄L鄄Trp)2鄄L鄄Lys鄄OCH3能诱导K562细胞凋亡,并且可能与细胞线粒体Δψm下降和ROS生成减少有; BACKGROUND & OBJECTIVE: Phosphorylation of protein and peptide plays an important role in life activity. Some phosphoryl peptides are found to have a ctivities to inhibit proliferation of tumor cells, but the involved mechanisms a re unclear. This study was designed to investigate cell apoptosis induced by (O, O-diisopropyl phosphoryl-L-tryptophan)2-L-lysine methyl ester <(DIPP-L-Trp)2-L-L ys-OCH3>, and its mechanism in K562 cells. METHODS: K562 cells were double stain ed by AnnexinV-FITC and propidium iodide (PI) to detect (DIPP-L-Trp)2-L-Lys-OCH3 -induced apoptosis by flow cytometry (FCM). After treatment of different concent rations of (DIPP-L-Trp)2-L-Lys-OCH3, K562 cells were stained by rhodamine123 and PI to detect changes in membrane potential (Δψm), or stained by 2',7'-dichlor ofluorescein diacetate (DCFH-DA) to detect reactive oxygen species (ROS) of mito chondrial by FCM. RESULTS: When treated with 50 μg/ml of (DIPP-L-Trp)2-L-Lys-OC H3 for 24 h, apoptosis rate of K562 cells was 61.9%, Δψm was decreased in 93.6 % of K562 cells,and ROS production was decreased. Both Δψm and ROS production in K562 cells mitochondria were decreased with the increasing concentration and extending treatment time of (DIPP-L-Trp)2-L-Lys-OCH3. CONCLUSION: (DIPP-L-Trp)2- L-Lys-OCH3 could induce apoptosis in K562 cells, which might relate with down-re gulation of mitochondrial Δψm and reduction of ROS production.; 国家自然科学基金重点项目(No.20472043); 清华工业研究院科技基金~~
语种中文 ; 中文
内容类型期刊论文
源URL[http://hdl.handle.net/123456789/60664]  
专题清华大学
推荐引用方式
GB/T 7714
刘峰,蒋宇扬,刘世英,等. 二异丙基磷酰化二肽甲酯通过线粒体途径诱导K562细胞凋亡[J],2010, 2010.
APA 刘峰.,蒋宇扬.,刘世英.,王凯.,曹健.,...&ZHAO Yu-Fen.(2010).二异丙基磷酰化二肽甲酯通过线粒体途径诱导K562细胞凋亡..
MLA 刘峰,et al."二异丙基磷酰化二肽甲酯通过线粒体途径诱导K562细胞凋亡".(2010).
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