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作 者:刘剑锋 冯伟 霍佳雯 魏大飞 潘德锋 LIU Jian-Feng;FENG Wei;HUO Jia-Wen;WEI Da-Fei;PAN De-Feng(Department of Pediatrics,The Second Affiliated Hospital,University of South China,Hengyang 421001,Hunan Province,China)
机构地区:[1]南华大学附属第二医院儿科,湖南衡阳421001
出 处:《中国实验血液学杂志》2020年第2期400-404,共5页Journal of Experimental Hematology
摘 要:目的:探讨汉防己甲素(Tetrandrine)靶向黏蛋白1(MUC1)诱导急性早幼粒细胞白血病(APL)细胞分化。方法:以HL-60细胞株作为研究对象,选取对数生长期细胞,分为空白对照、ATRA、汉防己甲素和ATRA+汉防己甲素,共4组。显微镜下观察各组细胞形态的变化;用NBT还原实验分析细胞分化能力的变化;采用流式细胞术检测细胞表面分化抗原CD11b表达的变化;采用Western blot检测MUC1表达的变化。结果:汉防己甲素可以诱导HL-60细胞分化;ATRA+汉防己甲素组NBT还原阳性率明显高于ATRA和汉防己甲素组(P<0.05);ATRA+汉防己甲素组CD11b+细胞百分率(43.62%±1.38%)明显高于汉防己甲素(15.25%±2.11%)、ATRA(21.84%±7.53%)和空白对照组(8.16%±1.01%)(P<0.05);汉防己甲素组MUC1蛋白量明显低于空白对照组和ATRA组(P<0.05)。结论:汉防己甲素体外能协同ATRA使HL-60细胞分化成熟,其作用机制可能与调控MUC1的表达有关。Objective:To investigate the differentiation of acute promyelocytic leukemia(APL)cells induced by Tetrandrine targeting MUC1.Methods:HL-60 cells at logarithmic growth phase were choosen as object of reaserch and were divided into four groups:control,ATRA,Tetrandrine and ATRA+Tetrandrine group.Cell morphologic changes in each group were observed by microscopy.The change of cell differentiation ability was analyzed by nitro-blue tetrazolium(NBT)reduction test.The expression of cell surface differentiation antigen CD11 b was measured by flow cytometry.The expression of MUC1 protein was detected by Western blot.Results:The differentiation of HL-60 cell could be induced by Tetrandrine.The NBT reduction-positive rate of ATRA+Tetrandrine group was significantly higher than that in ATRA group and Tetrandrine group(P<0.05).The percentage of CD11 b positive cells in ATRA+Tetrandrine group(43.62%±1.38%)was significantly higher than that in Tetrandrine group(15.25%±2.11%),ATRA group(28.84%±7.53%)and control group(8.16%±1.01%)(P<0.05).The content of MUC1 protein in Tetrandrine group was significantly lower than that in control group and ATRA group(P<0.05).Conclusion:Tetrandrine and ATRA can synergize to promote the differentiation and maturation of HL-60 cells,and the mechanism may be related with MUC1 expression.
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