中文摘要：

目的探讨肉桂醛氧氟沙星酰腙[N-（3-苯亚丙烯基）-6-氟-1，8-（2，1-丙氧基）-7-（4-甲基哌嗪-1-基）-喹啉-4（1H）-酮-3-甲酰肼，肉桂醛氧氟沙星酰腙]诱导人胰腺癌BxPC-3细胞凋亡的作用及机制。方法用不同浓度的肉桂醛氧氟沙星酰腙处理BxPC-3细胞，采用四甲基偶氮唑蓝（MTT）比色法，检测肉桂醛氧氟沙星酰腙对BxPC-3细胞的增殖抑制效应；采用形态学、TUNEL法和DNA琼脂糖凝胶电泳，检测细胞凋亡的发生；应用蛋白印迹技术检测凋亡相关基因caspase-3，caspase-8，caspase-9，bcl-2，bax和细胞色素C的表达。结果肉桂醛氧氟沙星酰腙在体外对BXPC-3细胞有显著增殖抑制效应，且呈浓度、时间依赖关系；在肉桂醛氧氟沙星酰腙作用下，BxPC-3细胞出现显著的细胞凋亡征象；Hoechst33258／PI荧光染色显示细胞固缩，核染色质聚集或断裂，形成凋亡小体；TUNEL实验统计细胞凋亡率显著高于对照组（P〈0．05）；琼脂糖凝胶电泳可见凋亡细胞典型的梯状DNA条带；肉桂醛氧氟沙星酰腙使凋亡相关基因bax、caspase-9和caspase-3蛋白表达增强，bcl-2表达降低，caspase-8、caspase-9活性裂解片段增加，线粒体细胞色素C降低，胞浆细胞色素C升高。结论凋亡是肉桂醛氧氟沙星酰腙杀伤肿瘤细胞的机制之一；肉桂醛氧氟沙星酰腙诱导胰腺癌BxPC-3细胞主要通过激活线粒体凋亡通路进行。

英文摘要：

OBJECTIVE To study the effect of cinnamaldehyde ofloxacin-3-ylhydrazone （ FQ16 ） on apoptosis of human pancreat- ic carcinoma cells in vitro. METHODS Human pancreatic carcinoma cell line BxPC-3 was treated with FQI6 at different concentra- tions. The proliferation inhibition was examined by MTF assay. Morphological examination, TUNEL and agarose gel electrophoresis method were used to detect apoptosis. Western blotting method was used to detect the expression of apoptosis related genes caspase-3, caspase-9, easpase-8, bel-2, bax and cytochrome C. RESULTS The cell proliferation was inhibited by FQ16 in a time- and a dose- dependent manner. Treatment of BxPC-3 cells with different concentrations of FQ16 for 24 h increased the percentage of the apoptotie cells obviously （ P 〈 0. 05 ） ; the morphology of BxPC-3 showed changes such as nuclear chromatin condensation and fragmentation and typical ladder DNA in apoptotic cells. FQ16 increased protein expression of bax, caspase-9 and caspase-3 , and induced cytosolic ac- cumulation of active caspase-9 and caspase-8, whereas the protein expression of bcl-2 decreased. Western blotting results reveal that FQ16 released mitochondrial cytochrome C into cytosol in a dose-dependent manner. CONCLUSION Apoptosis in pancreatic carci- noma BxPC-3 cells is one of the key mechanisms of action of cinnamaldehyde ofloxacin-3-ylhydrazone, and mitochondrial-dependent pathways are involved in the induction of apoptosis of BxPC-3 cells.