| Jing Liu,Haixia Li,Zhongcai Gao,Yuxia Wang,Wenqing Wei. Inhibitory effect of metformin on the proliferation of human hepatoma HepG2 cells and its potential mechanism. Oncol Transl Med, 2014, 13: 370-374. |
| 二甲双胍抑制人肝癌细胞HepG2的实验研究 |
| Inhibitory effect of metformin on the proliferation of human hepatoma HepG2 cells and its potential mechanism |
| Received:July 01, 2014 Revised:July 19, 2014 |
| DOI：10.1007/s10330-014-0027-y |
| 中文关键词: 二甲双胍；HepG2细胞；凋亡；cyclinD1；ROS |
| 英文关键词: metformin (MET); human hepaocellular carcinoma cell line HepG2; apoptosis; cyclin D1; reactive oxygen species (ROS) |
| 基金项目: |
| Author Name | Affiliation | Postcode | | Jing Liu | Department of Central Laboratory, General Hospital of Beijing Military Command, Beijing 100700, China | 100700 | | Haixia Li | Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China | | | Zhongcai Gao | Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China | | | Yuxia Wang | Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China | | | Wenqing Wei* | Department of Central Laboratory, General Hospital of Beijing Military Command, Beijing 100700, China | 100700 |
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| 中文摘要: |
| 目的：研究二甲双胍（MET）体外对人肝癌细胞HepG2细胞增殖的抑制作用及相关机制。方法：采用MTT法测定MET不同浓度、不同作用时间对HepG2细胞增殖的抑制作用；用流式细胞术检测HepG2细胞的凋亡；Western blot检测cyclinD1表达的变化；ROS荧光探针-DHE测定HepG2细胞中活性氧自由基（ROS）的含量。结果：MET具有抑制人肝癌细胞HepG2细胞增殖的作用，呈剂量和时间依赖性；MET促进HepG2细胞的凋亡；MET诱导HepG2细胞中ROS的生成；MET降低细胞周期蛋白的表达。结论：MET抑制人肝癌细胞增殖，诱导细胞凋亡，其机制可能与降低cyclinD1的表达和诱发ROS的生成有关 |
| 英文摘要: |
| Objective: This work aimed to study the inhibitory effect and the related mechanism of metformin (MET) on the proliferation of human hepatoma HepG2 cells. Methods: Human hepatoma HepG2 cells were treated with MET (0, 2, 10, and 50 mM). The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytometry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species (ROS) generated by HepG2 cells after treatment. Results: MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the production of ROS in HepG2 cells. Conclusion: MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation. |
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