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目的以紫杉醇处理的Jurkat细胞为模型,研究细胞自噬在儿童急性淋巴细胞白血病化疗过程中的作用。方法 10μg/ml的紫杉醇处理人急性T淋巴细胞白血病Jurkat细胞后,免疫印迹和流式细胞技术检测LC3β蛋白的表达变化,WST-1法检测PTX对Jurkat细胞的抑瘤率。结果 PTX处理Jurkat细胞0h、24h、48h后,抑瘤率分别为(4.2±1.2)%、(46.7±5.3)%、(65.9±9.4)%,组间比P均小于0.05;LC3β的平均荧光强度相对倍数分别(3.1±0.2)倍、(4.6±0.31)倍、(34.2±4.5)倍,组间比P值均小于0.05,与抑瘤率一样呈现时间依赖性增强;免疫印迹也显示PTX处理24h和48h后,LC3β的蛋白表达逐渐增强。结论细胞自噬在ALL化疗过程中活化,可导致化疗抵抗。
OBJECTIVE: To investigate the role of autophagy in the chemotherapy of childhood acute lymphoblastic leukemia using paclitaxel-treated Jurkat cells as a model. Methods The Jurkat cells were treated with paclitaxel (10μg / ml). The expression of LC3β protein was detected by Western blot and flow cytometry. The inhibitory rate of PTX on Jurkat cells was determined by WST-1 assay. Results The tumor inhibition rates of PTX-treated Jurkat cells were (4.2 ± 1.2)%, (46.7 ± 5.3)% and (65.9 ± 9.4)% respectively at 0h, 24h and 48h after treatment with PTX. The average fluorescence intensity of LC3β (3.1 ± 0.2) fold, (4.6 ± 0.31) fold and (34.2 ± 4.5) fold, respectively. The P values of the two groups were all less than 0.05, showing the same time-dependent enhancement as the tumor inhibition rate. Immunoblot also showed that PTX After 24h and 48h treatment, the protein expression of LC3β gradually increased. Conclusions Autophagy is activated during ALL chemotherapy and can lead to chemoresistance.