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作 者:司原[1] 王明明[1] 张伍魁[1] 谢强[2] 谢吉奎[2]
机构地区:[1]安徽医科大学核医学核医学教研室,合肥230032 [2]安徽省立医院PET-CT中心,合肥230001
出 处:《安徽医科大学学报》2010年第3期330-334,共5页Acta Universitatis Medicinalis Anhui
基 金:安徽省教育厅自然科学基金(编号:2006KJ3123);安徽医科大学校科研基金(编号:2007kj06)
摘 要:目的研究18F-FDG对HepG2肝癌细胞凋亡的影响,探讨其作用机制。方法将处于对数生长期的肝癌细胞分为实验组和对照组,以不同浓度18F-FDG处理HepG2肝癌细胞,用MTT法、流式细胞术和逆转录-聚合酶链式反应(RT-PCR)技术分别检测细胞增殖与凋亡、活性氧含量、rad51及p53基因表达的情况。结果 18F-FDG能诱导HepG2肝癌细胞凋亡,抑制其增殖,且随着18F-FDG浓度增大,凋亡细胞增加,活性氧产量增加,p53基因与rad51基因表达增强。结论 18F-FDG能诱导HepG2肝癌细胞凋亡,且凋亡率随药物活度浓度增大而增大。Objective To investigate the effects of ^18F-FDG on apoptosis of HepG2 cells and explone its possible mechanisms.Methods HepG2 liver cancer cell line was conventionally cultured.Cells during the stage of logarith-mic growth were divided into 18F-FDG treatment group and control group.MTT method,flow cytometry and reverse transcription-polymerase chain reaction(RT-PCR)were used to analyze the proliferation and apoptosis of cells,the quantity of reactive oxygen species and the expression of p53 gene and rad51gene induced by different radioactivity concentration of 18F-FDG,respectively.Results Apoptosis of HepG2 cells could be induced by ^18F-FDG,and the apoptosis rate and the production of reactive oxygen species increased and the expression of rad51 and p53 genes were enhanced with the increment of radioactivity concentrations of ^18F-FDG.Conclusion Apoptosis of HepG2 cells can be initiated by 18F-FDG,and their apoptosis rate increases with the radioactivity concentration of ^18F-FDG.
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