【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(COPADG)诱导的Eca-109细胞Caspase-3激活及细胞凋亡的影响,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,以COPADG及SP600125与细胞作用,细胞间接免疫荧光染色观察P-JNK蛋白表达的改变,流式细胞术检测细胞凋亡率及Caspase-3活性的变化。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,凋亡率明显减低,Caspase-3活性显著下调,与COPADG单作用组之间有显著性差异。结论:SP600125能够显著抑制COPADG诱导Eca-109细胞Caspase-3激活以及COPADG诱导Eca-109细胞凋亡,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。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 Caspase-3 activation of the human esophageal cancer cell line Eca-109 induced by the COPADG. and to discuss the possible molecular mechanisms in COPADG-induced apoptosis. Methods: The human esophageal caner cell line Eca-109 was cultured in vitro and was incubated with SP600125 and COPADG. The Changes in the expression of P-JNK was determined with immunofluorescence cytochemistry, apoptosis rate and Caspase-3 activity was analyzed using flow cytometry. Results: SP600125 remarkably reduced the expression of P-JNK and decreased apoptosis rate as well as Caspase-3 activity in the human esophageal cancer cell line Eca-109 compared with those treated with COPADG only. Conclusion: SP600125 has a significant inhibitory action on Caspase-3 activation and indirectly demonstrate a significant protective effect on the COPADG-induced apoptosis in Eca-109. Thus, JNK signaling pathway may play an important role in apoptosis of Eca-109 induced by the COPADG.更多还原