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5-溴粉防己碱与柔红霉素对K562/A02细胞凋亡及生存素表达的影响

[Effects of 5-bromotetrandrine and daunorubicin on apoptosis and expression of survivin in K562/A02 cells].

作者信息

Cai Xiao-Hui, Chen Bao-An, Cheng Jian, Wang Jun, Ding Jia-Hua, Bao Wen, Zhong Yue-Jiao, Gao Feng, Xu Wen-Lin, Shen Hui-Ling, Wei Hu-Lai, Chen Jing

机构信息

Department of Hematology, Medical School of Southeast University, Nanjing 210009, Jiangsu Province, China.

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Feb;19(1):24-7.

Abstract

The aim of this study was to investigate the potential benefit of combination therapy with 5-bromotetrandrine (5-BrTet) and daunorubicin (DNR) on chronic leukemia. The apoptosis of K562/A02 cells treated by DNA, BrTet and BrTet combined with DNR for 48 hours was detected by flow cytometry; the expressions levels of survivin mRNA and protein K562/A02 cells treated by DNR, BrTet and BrTet combined with DNR and in untreated K562 cells for 48 hours were measured by RT-PCR and Western blot respectively. The results showed that the combination of BrTet with DNR increased apoptotic rate of K562/A02, down-regulated the expression levels of survivin mRNA and protein in K562/A02 cells as compared with blank control and cells treated by BrTet or DNR alone, the survivin expression in K562/A02 cells was higher than that in K562 cells. It is concluded that the combination of BrTet with DNR can effectively reverse the multidrug resistance of K562/A02 cells, promote the apoptosis of K562/A02 cells, the mechanism of which may be related with down-regulation of survivin expression. Survivin may be a target for the treatment of MDR in hematopoietic malignancies.

摘要

本研究旨在探讨5-溴粉防己碱(5-BrTet)与柔红霉素(DNR)联合治疗对慢性白血病的潜在益处。采用流式细胞术检测DNA、BrTet以及BrTet与DNR联合处理K562/A02细胞48小时后的细胞凋亡情况;分别采用逆转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹法(Western blot)检测DNR、BrTet以及BrTet与DNR联合处理K562/A02细胞48小时以及未处理的K562细胞中生存素mRNA和蛋白的表达水平。结果显示,与空白对照组以及单独使用BrTet或DNR处理的细胞相比,BrTet与DNR联合使用可提高K562/A02细胞的凋亡率,下调K562/A02细胞中生存素mRNA和蛋白的表达水平,K562/A02细胞中的生存素表达高于K562细胞。结论:BrTet与DNR联合使用可有效逆转K562/A02细胞的多药耐药性,促进K562/A02细胞凋亡,其机制可能与下调生存素表达有关。生存素可能是治疗造血系统恶性肿瘤多药耐药的靶点。

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