摘要目的：探讨二十碳五烯酸（EPA）诱导人结肠癌SW480细胞凋亡的作用机制。方法体外培养SW480细胞，不同浓度 EPA 作用于 SW480细胞后，采用流式细胞仪检测 SW480细胞线粒体膜电位的变化，利用试剂盒检测细胞色素 C 含量变化，Western blot 法检测活化的 caspase-9和 caspase-3蛋白表达水平。结果经不同剂量 EPA（0μg／mL、42．1μg／mL、84．2μg／mL、168．4μg／mL）处理后，SW480细胞增殖受到明显抑制， EPA 呈剂量依赖性的诱导 SW480细胞线粒体膜电位下降，分别为（99．71±0．04）％、（95．04±0．10）％、（88．65±0．41）％、（73．60±1．20）％，与对照组相比，差异均有统计学意义（t ＝5．161、6．302、4．601、5．198，均P ＜0．05）。细胞浆中细胞色素 C 含量分别为（12．8±1．2）ng／mL、（115．5±3．5）ng／mL、（290．5±5．2）ng／mL、（262．0±12．5）ng／mL），均明显高于对照组，差异均有统计学意义（t ＝6．345、6．013、5．846、4．613，均 P ＜0．01）；随着 EPA 浓度的增加，活化 caspase-9和 caspase-3蛋白水平呈上调趋势。结论EPA 体外能够诱导SW480细胞发生凋亡，其作用机制主要通过线粒体介导的内源性凋亡途径，细胞色素 C 的释放，caspase-9和caspase-3蛋白活化。

abstractsObjective To investigate the effect of eicosapentaenoic acid(EPA)on the apoptosis of human colon cancer SW480 cells and the mechanisms.Methods Mitochondrial membrane potential was detected,the quan-tity of cytochrome C was analyzed by Elisa kit,and the expression of cleaved caspase -9 and caspase -3 was detected by Western Blot.Results After treatment with EPA (0μg/mL,42.1μg/mL,84.2μg/mL,168.4μg/mL),the mitochondrial membrane potential(Δψm)of SW480 cells were declined (P <0.05 ),the values were (99.71 ± 0.04)%,(95.04 ±0.10)%,(88.65 ±0.41)% and (73.60 ±1.20)%(t =5.161,6.302,4.601,5.198,all P <0.05).The quantity of cytochrome C in cytosol was increased significantly compared with no treatment group,and the values were (12.8 ±1.2)ng/mL,(115.5 ±3.5)ng/mL,(290.5 ±5.2)ng/mL and (262.0 ±12.5 )ng/mL in different EPA treatment groups(t =6.345,6.013,5.846,4.613,all P <0.01).The expression of cleaved caspase -9 and caspase -3 were significantly increased.Conclusion EPA inhibits SW480 cells growth and induces apoptosis in a dose dependent manner.This action may be mediated by mitochondria -mediated intrinsic apoptosis pathway,cyto-chrome C release,and caspase -9 and caspase -3 activation.