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目的 体外观察阿糖胞苷(1-β-D-arabinofuranosylcytosine, Ara-C)对肺腺癌A549细胞凋亡的诱导作用,探讨p53、p73基因在此凋亡过程中的调控作用.方法 Ara-C体外作用于A549细胞,TUNEL法检测A549细胞的凋亡;透射电镜观察A549细胞凋亡的典型超微结构;免疫印迹法检测Ara-C诱导A549细胞凋亡过程中p53、p73是否起到了凋亡调控的作用.结果 1.Ara-C作用A549细胞的实验组检测到大量的TUNEL阳性反应细胞,统计学分析实验组凋亡率与对照组相比有极显著性差异(P＜0.01);2.透射电镜观察到凋亡小体等典型的超微结构;3.免疫印迹法显示,Ara-C诱导A549细胞凋亡中p53蛋白表达量无变化,而p73蛋白表达量随A549细胞凋亡程度的增强而增加.结论 Ara-C明显诱导肺腺癌A549细胞凋亡而并非依赖于p53的调控作用;p73可能在Ara-C诱导A549细胞凋亡过程中发挥重要作用.“,”Objective To study the apoptosis pathway of human lung adenocarcinoma cell line A549 induced by 1-β-D-arabinofuranosylcytosine (Ara-C) in vitro. Methods A549 cells were incubated with Ara-C for 72hours in vitro. Biological changes of apoptotic cells were studied by TUNEL staining. Morphological changes of the A549 cells treated with Ara-C were observed by transmission electron microscope. The expressions of p53 and p73 were investigated by Western blotting. Results 1.Apoptotic rates of A549 cells exposure to Ara-C studied by TUNEL staining were higher than that of the control (P＜0.01). 2.Apoptosis body was apparently observed by transmission electron microscope. 3.Endogenous p73 but not p53 was induced and activated in dose-dependent manner upon Ara-C treatment by Western blotting.Conclusion Ara-C can effectively induce apoptosis of A549 cells. DNA damage-induced apoptosis of A549 cells treated by Ara-C is independent of functional p53.Up-regulation of p73 may play an important role that enhances the sensitivity of A549 cells to Ara-C and be partly responsible for p53-independent apoptosis.