| ZHANG Li-qun,MA Zeng-chun,WANG Yu-guang,et al.Radioprotective effect of E0703 on AHH-1 cells and the related mechanism[J].Chinese Journal of Radiological Medicine and Protection,2008,28(3):231-235 |
| Radioprotective effect of E0703 on AHH-1 cells and the related mechanism |
| Received:May 28, 2007 |
| DOI： |
| KeyWords:E0703 Ionizing radiation AHH-1 Cell cycle Radioprotection |
| FundProject: |
| Author Name | Affiliation | E-mail | | ZHANG Li-qun | Beijing Institute of Radiation Medicine, Beijing 100850, China | | | MA Zeng-chun | Beijing Institute of Radiation Medicine, Beijing 100850, China | | | WANG Yu-guang | Beijing Institute of Radiation Medicine, Beijing 100850, China | | | 肖成荣 | Beijing Institute of Radiation Medicine, Beijing 100850, China | | | 谭洪玲 | Beijing Institute of Radiation Medicine, Beijing 100850, China | | | 杨明会 | 解放军总医院 | | | 高月 | Beijing Institute of Radiation Medicine, Beijing 100850, China | gaoyue@yahoo.com |
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| Abstract:: |
| Objective E0703 is derived from estradiol and has anti-radiation effects on irradiated mice, the effects of E0703 on cell viability, cell cycle and the related mechanism in irradiated AHH-1 cells were investigated in this study. Methods Cell viability, cell apoptosis and cell cycle were determined by Cell Counting Kit-8, Annexin V-FITC double staining kit and Flow Cytometry, respectively. Level of mRNA and protein were detected by RT-PCR and Western blot, respectively. Results 3.0 Gy 60Coγ-rays induced significant cell cycle arrest, necrosis, apoptosis and reduction of viability. Pretreatment with E0703 for 12h before irradiation could increase cell viability and regulate cell cycle, but had no obvious effect on cell necrosis and apoptosis. The expression of cell cycle arrest related molecules Rb and MDM2 were increased after 3.0 Gy irradiation, but decreased significantly with pretreatment of E0703. Moreover, the phosphorylation of Rb was also increased. Conclusions The radioprotective function of E0703 might be exerted through influencing on cell cycle and promoting cell proliferation instead of apoptosis or necrosis. |
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