鱼藤素对人食管癌Ec-109细胞增殖及凋亡影响的实验研究

目的观察鱼藤素对人食管癌Ec-109细胞增殖及凋亡的影响并探讨其可能的作用机制。方法体外培养人食管癌Ec-109细胞，并将其分为空白对照组及5、10、20、40 nmol/L鱼藤素组5组。运用CCK-8法检测各组细胞24、48、72 h的增殖抑制情况；流式细胞仪检测各组24 h细胞早期凋亡率及24、48 h凋亡相关蛋白Bcl-2和Bax表达。结果与空白对照组同期比较，5、10、20、40 nmol/L鱼藤素组生长抑制率在24、48、72 h均增加，差异有统计学意义（P<0.05）。5、10、20、40 nmol/L鱼藤素组细胞早期凋亡率分别为（4.37±0.35）%、（6.71±0.14）%、（15.62±0.21）%及（19.78±0.15）%，与空白对照组自发早期凋亡率［（1.10±0.08）%］比较，差异均有统计学意义（P<0.05）。与空白对照组同期比较，10、20、40 nmol/L鱼藤素组Bcl-2蛋白表达明显下降，Bax蛋白表达明显上升，差异均有统计学意义（P<0.05）。上述指标均呈时间和剂量依赖性。结论鱼藤素对Ec-109细胞具有明显的抑制细胞增殖和促进细胞凋亡的作用，与上调Bax蛋白和使Bcl-2蛋白表达下降有关。

英文摘要:

Objective To observe the effects of deguelin on the apoptosis and proliferation of human esophageal cancer cell Ec-109， and to explore its possible mechanisms. Methods Human esophageal cancer cells Ec-109 were in vitro cultured. They were divided into the blank control group， and 5， 10， 20， and 40 nmol/L deguelin groups. The inhibition on the proliferation was detected at 24， 48， and 72 h using CCK-8 assay. The early apoptosis rate at 24 h was detected by flow cytometry. The expressions of apoptosis-related proteins Bcl-2 and Bax were detected at 24 and 48 h respectively. Results Compared with the blank control group at the same point， the growth inhibition rate in all deguelin groups increased at 24， 48， and 72 h， showing statistical difference （P<0.05）. The early apoptosis rate was 4.37%±0.35%， 6.71%±0.14%， 15.62%±0.21%， and 19.78%±0.15% in 5， 10， 20， and 40 nmol/L deguelin groups， respectively， showing statistical difference when compared with that of the blank control group （1.10%±0.08%， P<0.05）. Compared with the blank control group， Bcl-2 protein expression obviously decreased， and Bax protein expression obviously increased in 10， 20， and 40 nmol/L deguelin groups， showing statistical difference （P<0.05）. The aforesaid indices were in time- and dose-dependent manners. Conclusion Deguelin showed obvious effects on inhibiting the proliferation of Ec-109 cells and promoting their apoptosis， which was correlated with up-regulating Bax protein expression and down-regulating Bcl-2 protein expression.

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