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作 者:郭铁军[1] 白厚桥[1] 温培娥[1] 任海全[1] 张玉昆[1] 唐天华[1] 张灏[1] 毕高峰[1] 刘佳宁[1] 姜枫勤[1] 姜国胜[1]
机构地区:[1]山东省医学科学院基础医学研究所血液肿瘤室,济南250062
出 处:《国际肿瘤学杂志》2006年第4期300-303,共4页Journal of International Oncology
基 金:山东省自然科学基金资助项目(Z2004C08)
摘 要:目的检测急性早幼粒白血病细胞HL-60经过淫羊藿甙(ICA)诱导后信号传导与转录激活因子(STAT1、STAT3)和有丝分裂原激活蛋白激酶(p38MAPK、p42MAPK)表达变化在分化中的作用。方法建立ICA诱导分化模型,用瑞氏染色观察细胞形态,MTT实验测定细胞增殖的变化,NBT还原实验测定细胞分化状态,RT-PCR方法检测STAT1、STAT3、p38MAPK、p42MAPK 的mRNA的表达。结果 HL-60细胞经ICA作用24 h后,随着细胞增殖降低和分化的发生, p42MAPK的mRNA表达增加,STAT3的mRNA表达降低,STAT1和p38MAPK的mRNA未见明显的表达。结论 p42MAPK和STAT3与ICA诱导HL-60细胞分化有关,而p38MAPK和STAT1则与ICA诱导HL-60细胞分化无关。Objective To investigate the effect of signal transductors and activator of transcription( STATI and STAT3) as well as the mitogen-activated protein kinase( p38MAPK and p42MAPK) on differentiation of HL-60 cells induced by ICA. Methods The differentiation model was induced by ICA. The changes of cell morphology were observed by Wright staining, and the cell proliferation was determined by MTT experiment, the NBT reduction assay was used to detect the differentiation of HL-60 cells. The mRNA expressions of STAT1 ,STAT3 ,p38MAPK and p42MAPK in HL-60 cells exposed to ICA were assayed by semi-quantitative RT-PCR. Results ICA could up-regulate the mRNA expression of p42MAPK,but down-regulate those of STAT3, there was no obvious evidence to demonstrate the mRNA expression of p38MAPK and STAT1 in HL-60 cells. Conclusion p42MAPK and STAT3, but not p38MAPK and STAT1, are related to the induction of differentiation in HL-60 cells treated with ICA.
关 键 词:血液肿瘤 淫羊藿甙 信号传导 细胞分化 细胞外信号调节MAP激酶类
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