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维生素C增强氧化砷联用二甲萘醌诱导的U937细胞凋亡及其机制
引用本文:高飞,易静,史桂英,李慧,石学耕,王志伟,汤雪明. 维生素C增强氧化砷联用二甲萘醌诱导的U937细胞凋亡及其机制[J]. 中华血液学杂志, 2002, 23(1): 9-11
作者姓名:高飞  易静  史桂英  李慧  石学耕  王志伟  汤雪明
作者单位:上海第二医科大学细胞生物学教研室,200025
基金项目:国家自然科学基金资助项目 ( 39730 2 70 ),上海市教委高校科技发展基金资助项目 ( 2 0 0 0B10 1)
摘    要:目的 探讨维生素C是否可增强三氧化二砷(As2O3)联用二甲萘醌(DMNQ)对白血病细胞株U937的促凋亡效应及其机制。方法 以As2O3、维生素C、DMNQ不同组合孵育细胞,采用流式细胞仪及电镜检测细胞凋亡,并设立各种对照。结果 维生素C可增加As2O3联用DMNQ(10μmol/L)诱导U937细胞发生凋亡的比例(不加和加用维生素C细胞凋亡率分别为35.24%和61.20%);过氧化氢酶可逆转这一效应;维生素C对DMNQ(20μmol/L)单独诱导U937细胞凋亡无影响。结论 维生素C在As2O3存在的情况下,通过活性氧依赖的途径,促进U937细胞凋亡。

关 键 词:砷剂 抗坏血酸 细胞凋亡 活性氧组分 维生素C

Ascorbic acid enhances the apoptosis of U937 cells induced by arsenic trioxide in combination with DMNQ and its mechanism
GAO Fei,YI Jing,SHI Guiying,LI Hui,SHI Xuegeng,WANG Zhiwei,TANG Xueming. Laboratory of Cell Biology,Shanghai Second Medical University,Shanghai ,China. Ascorbic acid enhances the apoptosis of U937 cells induced by arsenic trioxide in combination with DMNQ and its mechanism[J]. Chinese Journal of Hematology, 2002, 23(1): 9-11
Authors:GAO Fei  YI Jing  SHI Guiying  LI Hui  SHI Xuegeng  WANG Zhiwei  TANG Xueming. Laboratory of Cell Biology  Shanghai Second Medical University  Shanghai   China
Affiliation:Laboratory of Cell Biology, Shanghai Second Medical University, Shanghai 200025, China.
Abstract:OBJECTIVE: To investigate whether ascorbic acid could enhance the efficacy of arsenic trioxide (As(2)O(3)) combined with 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) in inducing the apoptosis of leukemia cell line U937 and its possible mechanism. METHODS: Flow cytometry and electron microscopy were applied to detect apoptosis of U937 cells after treatment with various combinations of As(2)O(3), DMNQ and ascorbic acid for 24 hours. RESULTS: As(2)O(3) and DMNQ induced-apoptosis of U937 cells was enhanced (35.24%-->61.20%) upon cotreatment with ascorbic acid. Catalase could reverse this effect of DMNQ. Ascorbic acid had no effect on DMNQ-induced apoptosis of U937 cells. CONCLUSION: Ascorbic acid enhanced the apoptosis of U937 cells via reactive oxygen species-dependent pathway in the presence of As(2)O(3).
Keywords:Arsenictrioxide  Ascorbic acid  Cell apoptosis  Reactive oxygen species
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