喜树碱诱导鼻咽癌细胞凋亡的线粒体机制探讨

目的 :了解喜树碱 (CPT)诱导鼻咽癌细胞凋亡是否与线粒体膜电位改变有关。方法 :用 2 μmol/ L 的CPT 处理 CNE- 2 Z细胞 ,经流式细胞仪、Hoechst332 5 8/ PI双重染色鉴定凋亡细胞 ,同时用罗丹明 12 3(Rhodamine12 3)染色后 ,经流式细胞仪检测线粒体膜电位。结果 :CPT可明显降低线粒体膜电位 ,2 μm ol/ L 的CPT处理 CNE- 2 Z细胞 2 4h后 ,罗丹明 12 3摄取量低的细胞明显增加 ,达 (19.0± 3.0 ) % ,与 DMSO对照组的(7.0± 1.4) %相比 ,差异有显著性意义 (P <0 .0 5 )。结论 :降低线粒体膜电位可能是 CPT诱导鼻咽癌细胞凋亡的机制之一。

Mitochondrial mechanisms of CPT-induced apoptosis in nasopharygeal carcinoma cells

OBJECTIVE: To understand whether CPT-induced apoptosis is related to the alteration of mitochondrial transmembrane potentials (delta psi m). METHOD: A low differentiation human nasopharyngeal carcinoma (NPC) cell line of CNE-2Z cells were used as in vitro model. After treatment with 2 mumol/L CPT for 24 h, the delta psi m was detected by the staining of rhodamine 123 (Rh123), while apoptosis was confirmed by sub-G1 cell content and the double staining of hoechst33258 and propidium iodide (PI). RESULT: CPT induced delta psi m collapse and apoptosis. With 2 mumol/L CPT treatment for 24 h, delta psi mlow cell was increased to (19.0 +/- 3.0)%, while in the DMSO control, delta psi mlow was (7.0 +/- 1.4)% P < 0.05. CONCLUSION: The disruption of the delta psi m may be one of the mechanisms of CPT-induced apoptosis in CNE-2Z cells.