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雄黄诱导白血病细胞凋亡的研究
引用本文:赵新汉,全平,李晶,田洪刚,刘陕西. 雄黄诱导白血病细胞凋亡的研究[J]. 现代肿瘤医学, 2006, 14(1): 88-90
作者姓名:赵新汉  全平  李晶  田洪刚  刘陕西
作者单位:西安交通大学第一医院肿瘤内科,西安交通大学环境与疾病相关基因教育部重点实验室,陕西,西安,710061
摘    要:目的探讨雄黄对白血病细胞凋亡及Bc l-2表达水平的影响。方法以阿霉素作用组为阳性对照组,通过四甲基偶氮唑盐法(MTT)测定药物作用下细胞株的细胞活力(OD值),采用原位细胞凋亡检测法(TUNEL)观察凋亡细胞的形态学改变,用流式细胞仪法(FCM)测定药物作用下细胞株Bc l-2蛋白阳性表达率的变化。结果与ADR相比,雄黄作用组OD值和Bc l-2阳性表达率更低(P<0.05),凋亡率更高(P<0.05)。结论雄黄诱导白血病细胞凋亡的效果较好,且Bc l-2蛋白表达水平的变化能显著改变药物诱导细胞凋亡的能力。

关 键 词:雄黄  阿霉素  K562细胞株  Bcl-2  细胞凋亡
文章编号:1672-4992-(2006)01-0088-03
收稿时间:2005-05-25
修稿时间:2005-08-25

Research on the cell apoptosis of leukemia Induced by arsenic sulfide
ZHAO Xin -han, QUAN Ping, LI Jing,et al.. Research on the cell apoptosis of leukemia Induced by arsenic sulfide[J]. Journal of Modern Oncology, 2006, 14(1): 88-90
Authors:ZHAO Xin -han   QUAN Ping   LI Jing  et al.
Affiliation:ZHAO Xin -han, QUAN Ping, LI Jing, et al.
Abstract:Objective To observe the cell apoptosis of leukemia and the Bcl-2 protein expression level under the action of arsenic sulfide.Methods The cell strain affected by ADR was used to be positive contrast.The 3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyl-tetrazolium bromide(MTT) method was used to measure the cell survival(OD value) of cell strain under the action of ADR and arsenic sulfide.The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) method was used to observe the morphological change of the apoptotic cells and the flow cytometry(FCM) method was used to measure the change of the Bcl-2 positive expression rate of cell strain under the action of ADR and arsenic sulfide.Results Compared to those affected by ADR,the OD value and Bcl-2 protein expression level of the K562 cell strain affected by arsenic sulfide were even lower(P<0.05),the apoptotic rate was even higher(P<0.05).Conclusion The apoptotic result induced by arsenic sulfide is better and the change of the Bcl-2 protein expression level is able to notably change the ability of drugs to induce cell apoptosis.
Keywords:realgar  adriamycin  K562 cell strain  Bcl-2  cell apoptosis
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