过氧化氢在乙醇抑制肝癌细胞增殖中的作用

The Role of H_2O_2 on Ethanol Suppress Hepatocellular Carcinoma Proliferation

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 study the role of H2O2 on ethanol suppress hepatocellular carcinoma(HCC) proliferation. Methods After 40 mmol/L ethanol acted on HCC line SMMC-7721 ,the cell was counted respectively after 12 h,24 h,48 h. H202 .mitochondrial membrane potential and apoptotic sub-G1 peak was detected by flow cytometer when CAT was added or not. Results The proliferation of SMMC-7721 cells was suppressed, it was 85.44 ±2.97% after 48 h.H2O2 ascended to 6. 32± 0.93% after half a hour,it was 25. 68 ?.67% and 98.78 ±3,65% after one hour and two hours respectively;mitochondrial membrane potential was damaged after 6 hours; apoptotic sub-G1 peak was happened after 24 h. CAT can reduce these changes. Conclusion Ethanol suppressed SMMC-7721 cells proliferation was caused by ascending H2O2 which damaged mitochondrial membrane potential and induced SMMC-7721 cells apoptosis.