龙群,肖潇,宋晶睿,饶青,刘晟,何志旭,李艳梅
LONG Qun,XIAO Xiao,SONG Jingrui,RAO Qing,LIU Sheng,HE Zhixu,LI Yanmei

• 1:贵州医科大学基础医学院免疫教研室&组织工程与干细胞实验中心
• 2:贵州医科大学省部共建药用植物功效与利用国家重点实验室
• 3:贵州省中国科学院天然产物化学重点实验室

摘要(Abstract)：

目的:研究Calothrixin B衍生物L20对白血病K562细胞的抑制作用及其机制。方法:采用四唑盐(MTT)法检测化合物L20对K562细胞的抑制作用,使用流式细胞分析仪检测化合物L20对K562细胞凋亡及周期的影响,用DCFH-DA标记的荧光探针通过荧光显微镜观察活性氧(ROS)的改变,Western蛋白印迹检测相关蛋白的表达。结果:L20处理后的K562细胞增殖受到明显抑制,L20能够诱导K562细胞凋亡,并使其细胞周期阻滞在G_2/M期,L20还可以使ROS在K562细胞中堆积;在蛋白水平上L20能够下调p-ERK、BCL-2和pCDC25C,上调BAX、p-CDK1及CDC25C,并激活Caspase家族。结论:L20具有通过MAPK通路诱导K562细胞凋亡及将细胞周期阻滞在G_2/M期的活性。
Objective: To study the inhibitory effect and its mechanism of Calothrixin B derivative-a compound L20 on leukemia K562 cells. Methods: MTT assay was used to detect the growth inhibitory effect of compound L20 on K562 cells. Flow cytometry was used to compound L20-mediated apoptosis and cell cycle. Reactive oxygen species( ROS) was observed with a microscope. Western blot was used to detect protein expression levels. Results: Compound L20 significantly inhibited the proliferation of K562 cells,induced apoptosis and blocked the cell cycle in G_2/M phase. In addition,compound L20 led to ROS accumulation in K562 cells. Furthermore,compound L20 downregulated pERK,BCL-2 and p-CDC25 C,upregulated BAX,p-CDK1 and CDC25 C,and activated the Caspase family. Conclusion: Compound L20 induces the apoptosis of K562 cells through the MAPK pathway and blocks the cell cycle in G_2/M phase.

关键词(KeyWords)： 白血病;Calothrixins B;K562细胞;凋亡;G2/M期;MAPK通路
leukemia;calothrixin B;K562 cells;apoptosis;G2/M phase;MAPK pathway

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金项目(81872772、81960546、U1812403-4);; 贵州省科技计划项目[黔科合平人才(2019)5406、QKH20181409、QKH20192762、QKH20205008]

作者(Author): 龙群,肖潇,宋晶睿,饶青,刘晟,何志旭,李艳梅
LONG Qun,XIAO Xiao,SONG Jingrui,RAO Qing,LIU Sheng,HE Zhixu,LI Yanmei

DOI: 10.19367/j.cnki.2096-8388.2020.05.001

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