依托泊甙（VP—16）诱导人肺腺癌细胞凋亡

目的探讨ＶＰ－１６对肺腺癌细胞凋亡的诱导作用。方法采用光镜、电镜、流式细胞仪、凝胶电泳和ＴｄＴ原位末端标记法检测ＶＰ－１６诱导人肺腺癌ＡＧＺＹ－８３－α细胞凋亡规律，并观察放线菌酮对凋亡的抑制程度。结果ＶＰ－１６在显著抑制细胞增殖的同时，能够诱导细胞凋亡，将细胞阻滞于Ｇ２期。放线菌酮对凋亡有显著的抑制作用。结论ＶＰ－１６诱导细胞凋亡，是其杀死肿瘤细胞的重要机制之一。该凋亡具有明显的时间和剂量依赖性。

Induction of Apoptosis by Etoposide (VP-16) in Human Lung Adenocarcinoma Cells

Objectives To shed light upon the induction of apoptosis by Etoposide (VP-16) in lung cancer cells. Methods With the use of fluorescence microscopy, electron microscopy, flow cytometry,DNA gel electrophoresis and TdT-mediated dUTP-biotin nick end labelling (TUNEL), induction of apoptosis by VP-16 was investigated and the inhibition of DNA fragmentation by l g/ml cycloheximide was examined on 1.5% agarose gel electrophoresis. WTHZResults VP-16 not only caused significant growth inhibition, but also induced extensive apoptosis. When examined by light microscopy and electron microscopy, the dead cells showed morphological characteristics of apoptosis. DNA fragmentation was detected on electrophoresis and was markedly suppressed by cycloheximide, indicating that cycloheximide provided protection from VP-16 induced cytotoxicity. DNA histogram of flow cytometry showed increased apoptotic peak (Ap peak), and cells were arrested in G2 phase. ConclusionZThe induction of apoptosis by VP-16 may play a key role in its antineoplastic effect. The mode of cell death is dependent on the concentration of the agent used and the time of cell exposure.