| 周永,糜漫天,杨镇洲,朱俊东,许红霞.三羟异黄酮对正常和辐射损伤小鼠骨髓造血细胞周期的影响[J].中华放射医学与防护杂志,2006,26(5):434-437 |
| 三羟异黄酮对正常和辐射损伤小鼠骨髓造血细胞周期的影响 |
| Effect of genistein on cell cycle of bone marrow hematopoietic cells in normal and irradiated mice |
| 投稿时间：2005-12-28 |
| DOI： |
| 中文关键词: 三羟异黄酮 骨髓造血细胞 细胞周期 bcl-2 |
| 英文关键词:Genistein Bone marrow hematopoietic cells Cell cycle bcl-2 |
| 基金项目:国家自然科学基金资助项目(30100046) |
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| 中文摘要: |
| 目的 三羟异黄酮(genistein,GEN)对正常和辐射损伤小鼠骨髓造血细胞(bonemarrowhematopoieticcell,BMHC)的细胞周期、增殖能力及bcl-2基因表达的影响,以期阐明其防护放射性造血损伤的分子机制。方法 照射前24h,GEN以160mg/kg体重剂量给予小鼠灌胃,流式细胞仪观察BMHCs细胞周期及增殖能力变化,RT-PCR及Westernblot方法分析BMHCsbcl-2mRNA和蛋白表达情况。结果 ①GEN可诱导正常小鼠BMHCs细胞周期一过性改变,即给药后1d,BMHCs增殖抑制,大量细胞阻滞于G0/G1期;给药后2d,GEN诱导BMHCs由G0/G1期向S期转换,S期细胞明显增多;4d后逐渐恢复正常。②照射前24h给药,GEN可减少射线导致的BMHCs增殖抑制,使照后阻滞于G0/G1期细胞减少;S期和G2/M期细胞增多,细胞增殖能力较强。同时,GEN预处理组bcl-2mRNA及蛋白的表达均较高。结论 改变BMHCs细胞周期、降低BMHCs的辐射敏感性、抑制BMHCs凋亡和提高残留BMHCs的增殖分化能力可能是GEN防护放射线造血损伤的分子机制之一。 |
| 英文摘要: |
| Objective To study the effects of genistein on cell cycle, proliferation and expression of bcl-2 gene in bone marrow hematopoietic cells (BMHCs) of normal and irradiated mice in order to explore mechanisms for protection of genistein from radiation-induced hematopoietic system injury. Methods Adult male BALB/c mice were orally administered with genistein (160 mg/kg b.w.) 24 h before irradiation. Cell cycles in BMHCs of the normal and irradiated mice were measured by flow cytometry. The protein and mRNA expressions of bcl-2 gene in BMHCs were analyzed by Western blot and RT-PCR, respectively. Results a) Transitory and significant changes occurred in the cell cycle of BMHCs in the normal mice after administration of genistein: first, the proliferation suppression of BMHCs was observed and most cells were arrested in G0/G1 phase on day 1; second, progression of cells from G0/G1 phase into S phase was observed, accumulation of cells in S phase on day 2, and back to the normal level on day 4. b) Genistein, administration 24 h before irradiation, decreased the percentage of BMHCs in G0/G1 phase and increased cell proliferation. Moreover, genistein up-regulated the protein and mRNA expressions of bcl-2 in BMHCs in the irradiated mice. Conclusions It was shown that changing with cell cycle, strengthening of radioresistant, suppressing of radiation-induced apoptosis, and enhancing of proliferation and differentiation of BMHCs maybe the underlying mechanisms for genistein protection of hematopoietic system against radiation damage. |
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