摘要
目的探讨反式桂皮醛(TCA)对慢性髓细胞白血病细胞K562的诱导分化作用及其机制。方法以低浓度TCA(60μmol/L)作用于体外培养的K562细胞,流式细胞术检测细胞周期、细胞凋亡率和细胞表面抗原表达,Real-time PCR技术检测K562细胞bcr-abl融合基因转录水平,免疫印迹法检测K562细胞的CrkL和p38MAPK磷酸化水平。结果低浓度TCA作用后,K562细胞表面单核细胞分化抗原CD11b和CD14表达明显增加,细胞阻滞于G2/M期。随TCA作用时间延长,K562细胞凋亡增加。K562细胞分化过程中,bcr-abl基因转录水平明显下降,CrkL蛋白磷酸化明显受抑,p38MAPK磷酸化水平增加。结论低浓度TCA诱导K562细胞向单核细胞分化,分化的K562细胞易于凋亡。低浓度TCA诱导K562细胞分化与细胞周期受阻、bcr-abl融合基因表达和功能受抑及p38MAPK活化有关。
Objective To explore the differentiation-inducing effect of trans-cinnamaldehyde（TCA）on chronic myeloid leukemic（CML）cells K562 and its mechanism.Methods K562 cells were treated with low concentration of TCA（60μmol/L）.The differentiation markers on the cell surface,the cell cycle and apoptosis of K562 cells were detected by flow cytometry.Real-time polymerase chain reaction（RT-PCR）was used to detect the transcription level of bcr-abl mRNA in K562 cells and Western blotting to determine the phosphorylation of CrkL and p38 MAPK.Results Low concentration of TCA enhanced the expression levels of the monocytic differentiation markers CD11 band CD14on K562 cells,and arrested the cells at G2/M phase.With drug-induced time increasing,the apoptosis rate of K562 cells was increased.The expression level of bcr-abl mRNA and the phosphorylation level of CrkL were significantly decreased in differentiated K562 cells,with the phosphorylation level of p38 MAPK increasing.Conclusion Treatment with low concentration of TCA induced monocytic differentiation of K562 cells and differentiated cells were prone to apoptosis.TCA-induced differentiation of K562 cells was related to cell cycle arrest,the inhibition of the expression and function of bcr-abl gene and the p38 MAPK activation.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2015年第6期678-681,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
深圳市科技局资助项目(No.201303188)
深圳市南山区政府资助项目(No.2010003)
