【摘要】 目的观察特异性C-JUN氨基末端激酶(JNK)抑制剂SP600125对D-氨基葡萄糖衍生物2-(3-羧基-1-丙酰氨基)-2-脱氧-D-葡萄糖(COPADG)诱导的Eca-109细胞凋亡和细胞周期阻滞的影响,并探讨COPADG诱导Eca-109细胞凋亡的潜在分子机制。方法体外培养Eca-109细胞,以COPADG及SP600125与细胞作用;Western blot法检测P-JNK蛋白表达,MTT法检测细胞增殖,流式细胞术检测细胞周期。结果COPADG显著增加Eca-109细胞P-JNK蛋白的表达和细胞凋亡率,且诱导Eca-109细胞发生G0/G1期细胞阻滞,SP600125明显减少Eca-109细胞凋亡,并使G0/G1期细胞阻滞向G2/M期细胞阻滞发展。结论COPADG可能通过激活JNK信号通路诱导Eca-109细胞凋亡。更多还原

【Abstract】 Objective To explore the effect of SP600125,a specific C-JUN NH2 terminal protein kinase(JNK) inhibitor,on apoptosis and cell-cycle arrest of the human esophageal cancer cell line Eca-109 induced by 2-(3-carboxy-1-oxopropyl)amino-2-deoxy-D-Glucose(COPADG)and potential molecular mechanism in COPADG-induced cell apoptosis was discussed.Methods Eca-109 cells were cultured and then pre-incubated with SP600125 for 30 min prior to exposure to COPADG of different concentrations and for different times.Changes of expression of P-JNK protein were examined by Western blot;Cell growth inhibitory rate was detected by MTT colorimetric assay;Apoptosis and cell-cycle arrest were analyzed by flow cytometry.Results COPADG significantly inhibited prolifer-ation of Eca-109 cells and induced them into apoptosis and cell-cycle arrest in G0/G1 phase.Western blot showed that the protein expression of P-JNK was increased in a dose-dependent manner in Eca-109 cells after stimulation by COPADG.SP600125 remarkablely inhibited the protein expression of P-JNK as well as the apoptosis rate and cell growth inhibitory rate in Eca-109 cells induced by COPADG as compared with those treated with only COPADG,meanwhile,cell-cycle arrest in G0/G1 phase progressed to cell-cycle arrest in G2/M phase.Conclusion JNK signaling pathway may play an important role in apoptosis of Eca-109 induced by the COPADG.更多还原