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目的:探讨和厚朴酚(honokiol,HNK)对人急性髓性白血病KG1a细胞凋亡的影响及其可能的机制。方法:XTT法检测不同质量浓度HNK对KG1a细胞增殖的影响,流式细胞术检测不同质量浓度HNK作用后KG1a细胞的细胞周期及凋亡,RT-PCR法检测KG1a细胞Bcl-2、Bid、Bax、Bak、Bad、P53、NF-κB等凋亡相关基因的表达。结果:HNK(2.5、5、8、10、15、20、40μg/ml)对KG1a细胞的增殖有明显抑制作用,且呈时间和剂量依赖性(P<0.01),其中24、48 h的半数抑制浓度(IC50)分别为10.23、8.25μg/ml。流式细胞术结果显示,经HNK(5、10μg/ml)处理后,KG1a细胞被阻滞在G0/G1期,早期凋亡率分别为(11.16±1.27)%和(21.46±3.13)%,显著高于对照组的(6.03±1.10)%(P<0.01)。RT-PCR检测结果显示,HNK(10μg/ml)处理后KG1a细胞内促凋亡基因Bax表达显著上调,Bad轻度上调;抗凋亡基因NF-κB表达显著下调。结论:HNK能诱导人急性髓性白血病KG1a细胞凋亡,其机制可能与Bax、Bad基因表达上调及NF-κB基因表达下调有关。
Objective: To investigate the effect of honokiol (HNK) on the apoptosis of human acute myeloid leukemia cell line KG1a and its possible mechanism. Methods: The effect of different concentration of HNK on the proliferation of KG1a cells was detected by XTT method. The cell cycle and apoptosis of KG1a cells were detected by flow cytometry. The expressions of Bcl-2, Bid, Bax , Bak, Bad, P53, NF-κB and other apoptosis-related genes. Results: HNK (2.5, 5, 8, 10, 15, 20, 40μg / ml) significantly inhibited the proliferation of KG1a cells in a dose- and time- Inhibitory concentration (IC50) were 10.23,8.25μg / ml. Flow cytometry showed that KG1a cells were arrested in G0 / G1 phase after treatment with HNK (5, 10μg / ml), the early apoptosis rates were (11.16 ± 1.27)% and (21.46 ± 3.13)%, Significantly higher than that of the control group (6.03 ± 1.10)% (P <0.01). The results of RT-PCR showed that the expression of Bax in KG1a cells was significantly up-regulated after treatment with HNK (10μg / ml), and Bad was slightly increased. The expression of anti-apoptotic gene NF-κB was significantly down-regulated. CONCLUSION: HNK can induce KG1a cell apoptosis in human acute myeloid leukemia. The mechanism may be related to up-regulation of Bax and Bad genes and down-regulation of NF-κB gene expression.