SP600125对D-氨基葡萄糖衍生物诱导Eca-109细胞凋亡的影响

Effect of SP600125 on apoptosis of cell line Eca-109 induced by COPADG

目的:观察特异性JNK抑制剂[specificc-junNH2terminalproteinkinase(JNK)inhibitor]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{[2-(3-carboxy-1-oxopropyl)a-mino-2-deoxy-D-Glucose],COPADG}诱导Eca-109细胞凋亡的影响并探讨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,用COPADG及SP600125对细胞进行处理。细胞间接免疫荧光染色观察P-JNK蛋白表达的改变,倒置相差显微镜观察细胞形态学变化;MTT检测不同时间点的细胞活性;流式细胞术检测细胞凋亡率。结果:经SP600125处理后,COPADG诱导的Eca-109细胞P-JNK蛋白表达明显减弱,同时,COPADG诱导的Eca-109细胞凋亡率明显减低,细胞增殖抑制率下降明显,与COPADG单独作用组之间比较差异有统计学意义。结论:SP600125对D-氨基葡萄糖衍生物CO-PADG诱导Eca-109细胞凋亡具有抑制作用,并间接证明JNK信号转导通路在COPADG诱导Eca-109细胞凋亡过程中发挥着重要作用。

OBJECTIVE： To explore the effect of SP600125, a specific c-jun NH2 terminal protein kinase （JNK） inhibitor, on apoptosis of human esophageal cancer cell line Eca-109 induced by the COPADG and the possible molecular mechanisms in COPADG-induced cell apoptosis. METHODS： The human esophageal cancer cell line Eca-109 was cultured in vitro, and incubated with SP600125 and COPADG. Changes in the expression of P-JNK were determined with immunofluorescence cytochernistry, and the cellular morphological changes were observed by inverted phase contrast microscopy. Cell viability was detected by MTT, and apoptosis rate was analyzed by using flow cytometry. RESULTS： SP600125 significantly reduced the expression of P-JNK and decreased apoptosis rate as well as growth inhibition in the human esophageal cancer cell line Eca-109 compared with those treated with only COPADG. CONCLUSIONS：SP600125 has a significant inhibitory effect on the COPADG-induced apoptosis and cell viability decrease in Eca-109; JNK signaling pathway may play an important role in apoptosis of Eea-109 induced by the COPADG.