论文部分内容阅读
目的探讨过氧化氢(H2O2)在乙醇抑制肝癌细胞增殖过程中的作用。方法40mmol/L低浓度乙醇作用于人肝癌细胞株SMMC-7721,分别于12h、24h、48h后观测细胞增殖情况。流式细胞仪检测H2O2、线粒体膜电位和细胞亚二倍体凋亡峰情况,比较乙醇组与乙醇合用过氧化氢酶(CAT)组两组之间线粒体膜电位改变及细胞亚二倍体凋亡峰变化情况。结果乙醇能抑制SMMC-7721细胞增殖,在48h后细胞抑制率达B5.44±2.97%。细胞内H2O2在乙醇作用30min后增加不明显(6.32±0.93%),1h后明显增加(25.68±1.67%),2h后增加非常明显(98.78±3.65%)。乙醇作用6h后线粒体膜电位出现降低,24h后检测到细胞亚二倍体凋亡峰出现。CAT能抑制上述两指标改变,差异均有显著性。结论乙醇能够抑制SMMC-7721细胞增殖,其作用机制和H2O2损伤SMMC-7721细胞线粒体,诱导细胞凋亡有关。
Objective To investigate the role of hydrogen peroxide (H2O2) in inhibiting the proliferation of hepatoma cells induced by ethanol. METHODS: Human hepatocellular carcinoma cell line SMMC-7721 was treated with 40 mmol / L ethanol. The cell proliferation was observed at 12h, 24h and 48h respectively. The changes of mitochondrial membrane potential and mitochondrial apoptotic peak were detected by flow cytometry. The changes of mitochondrial membrane potential and mitochondrial apoptosis were compared between ethanol group and ethanal combined with catalase (CAT) Death peak changes. Results Ethanol could inhibit the proliferation of SMMC-7721 cells, and the cell inhibitory rate reached 48.44 ± 2.97% after 48h. The intracellular H2O2 did not increase significantly after ethanol exposure for 30 min (6.32 ± 0.93%), significantly increased after 1 h (25.68 ± 1.67%), and significantly increased after 2 h (98.78 ± 3.65%). The mitochondrial membrane potential decreased after 6 hours of ethanol exposure, and the sub-diploid apoptotic peak appeared after 24 hours. CAT can inhibit the above two indicators change, the difference was significant. Conclusion Ethanol can inhibit the proliferation of SMMC-7721 cells, and its mechanism is related to the damage of mitochondria induced by H2O2 in SMMC-7721 cells and the induction of apoptosis.