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作 者:王明明[1] 司原[1] 邱俊[1] 谢强[2] 谢吉奎[2]
机构地区:[1]安徽医科大学核医学教研室,合肥230032 [2]安徽省立医院PET-CT中心,合肥230001
出 处:《辐射研究与辐射工艺学报》2010年第6期357-362,共6页Journal of Radiation Research and Radiation Processing
基 金:安徽省教育厅自然科学基金(2006KJ123)资助
摘 要:为研究18F-FDG对HepG2肝癌细胞增殖的影响,探讨其作用机制,以0—92.5×106 Bq/mL的18F-FDG作用HepG2肝癌细胞后6、12和24 h,用倒置显微镜观察、流式细胞术和逆转录-聚合酶链式反应(RT-PCR)技术检测细胞增殖、凋亡、活性氧含量及P53基因表达。结果表明,18F-FDG能诱导HepG2肝癌细胞的凋亡,并随18F-FDG放射性浓度的增大,细胞凋亡率增大,活性氧含量增加,P53表达增强。由此可见,18F-FDG能通过诱发HepG2肝癌细胞凋亡来抑制其增殖,且抑制率呈放射性浓度依赖性升高。The influence of 18F-FDG on the proliferation of HepG2 liver cancer cell was investigated and related possible mechanism was elucidated in this paper.HepG2 liver cancer cells were conventionally cultured.The cells during the phase of logarithmic growth were divided into different groups of 18F-FDG treatment and control groups.At 6,12 and 24h after treatment of 0—92.5×106Bq/mL of 18F-FDG,inverted microscopy,the cell apoptosis was analyzed by use of flow cytometry and reverse transcription-polymerase chain reaction to analyze meanwhile the content of reactive oxygen species(ROS) and expression of p53 gene in cells induced by 18F-FDG,were determined respec-tively.After exposure to 18F-FDG,the apoptotic morphological changes of HepG2 liver cancer cells were observed.It was found that inhibition rate of cell proliferation,production of ROS and apoptosis rate increased with the radio-activity concentration of 18F-FDG in the range of 0—92.5×106Bq/mLwhile the expression of p53 gene increased gradually.The results indicate that 18F-FDG may inhibit the proliferation of HepG2 liver cancer cells by apoptosis and increment of inhibition rate.
关 键 词:18氟-氟代脱氧葡萄糖 HEPG2肝癌细胞 细胞增殖 细胞凋亡
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