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. 2019 Dec;27(6):1761-1766.
doi: 10.19746/j.cnki.issn.1009-2137.2019.06.009.

[Primary Mechanisms of CD34+CD38---KG1a Leukemia Stem Cells Apoptosis Induced by FA-2-b-β Extracted from Qinba Selenium- Mushroo]

[Article in Chinese]
Affiliations

[Primary Mechanisms of CD34+CD38---KG1a Leukemia Stem Cells Apoptosis Induced by FA-2-b-β Extracted from Qinba Selenium- Mushroo]

[Article in Chinese]
Dong-Ping Wang et al. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2019 Dec.

Abstract

Objective: To investigate the apoptosis of CD34+CD38--KG1a leukemia stem cells induced by Qinba selenium-mushroom extract(FA-2-b-β), and its related mechanism.

Methods: CD34+CD38---KG1a cells were isolated from KG1a cell line by magnetic activated cell sorting. The proliferation ability of KG1a stem cells treatd by various concentration of FA-2-b-β(1.2-2.4 mg/ml) in vitro for 24 and 48 hours were tested by cell counting Kit-8(CCK8). Flow cytometry was used to detect the apoptosis rate of KG1a stem cells in each group after treated by FA-2-b-β in vitro. Expression of BAX,BCL-2,Casepase-3 and Cyclin D1 protein were detected by Western blot.

Results: The proportion of CD34+CD38---KG1a stem cells was (95.35±2.63)% after immunomagnetic isolation. The proliferation of KG1a stem cells was inhibited significantly by FA-2-b-β, which shows a time- and dose-dependent manner (24 h,r=0.943; 48 h,r=0.976). Flow cytometry shows that with the increasing of drug concentration, the apoptosis was also increased, when KG1a stem cells was treated by FA-2-b-β for 24 h. Western blot indicated that the expression of apoptosis-related protein BAX and Casepase-3 were up-regulated, the expression of BCL-2 and Cyclin D1 were down-regulated.

Conclusion: FA-2-b-β can regulate proliferation and apoptosis KG1a stem cells, the involved mechanism may be related with the activation of mitochondrial-mediated apoptotic pathway.

题目: 秦巴硒菇提取物FA-2-b-β诱导CD34+CD38---KG1a白血病干细胞凋亡及其相关机制.

目的: 探讨秦巴硒菇提取物FA-2-b-β对CD34+CD38---KG1a白血病干细胞凋亡的诱导及其相关机制.

方法: 用免疫磁珠分选法从KG1a细胞株中分选出CD34+CD38---KG1a干细胞;不同浓度的FA-2-b-β(1.2-2.4 mg/ml)体外干预KG1a干细胞24、48 h,应用CCK-8检测其增殖能力变化;流式细胞术检测FA-2-b-β干预KG1a干细胞后各组细胞凋亡比例;采用Western blot检测BAX、BCL-2、Casepase-3及Cyclin D1蛋白表达.

结果: 经过免疫磁珠分选后KG1a干细胞比例为(95.35±2.63)%。FA-2-b-β对KG1a干细胞的增殖具有明显抑制作用,呈时间和剂量依赖性(24 h,r=0.943;48 h,r=0.976)。流式细胞术检测显示,不同浓度FA-2-b-β作用KG1a干细胞24 h时,随药物浓度增加凋亡率也随之增高。Western blot检测显示,凋亡相关蛋白BAX和Casepase-3表达上调,BCL-2和Cyclin D1的表达下调.

结论: 秦巴硒菇提取物FA-2-b-β能够调控KG1a干细胞的增殖和凋亡,其抗肿瘤效应可能通过调控线粒体介导的凋亡途径实现.

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