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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。
Objective To investigate the effects of genistein (GEN) on the cell cycle, proliferation and bcl-2 gene expression in bone marrow hematopoietic cells (BMHCs) of normal and radiation-injured mice in order to clarify the molecular mechanism of protection against radiation-induced hematopoietic damage . Methods 24h before genotoxicity, GEN was administered intragastrically at a dose of 160mg / kg body weight. The cell cycle and proliferative capacity of BMHCs were observed by flow cytometry. The mRNA and protein expression of Bcl-2 and Bcl-2 in BMH were analyzed by RT-PCR and Western blotting. Results ①GEN induced a transient change in the cell cycle of BMHCs in normal mice, that is, 1 h after administration, the proliferation of BMHCs was inhibited and a large number of cells were arrested in G0 / G1 phase. At 2 days after administration, GEN induced BMHCs from G0 / G1 phase to S Period conversion, S phase cells increased significantly; 4d gradually returned to normal. ② 24h before irradiation, GEN can reduce the radiation-induced inhibition of proliferation of BMHCs, so that cells in G0 / G1 phase after irradiation were reduced; cells in S phase and G2 / M phase increased, and cell proliferation ability was stronger. At the same time, the expression of bcl-2 mRNA and protein in GEN pretreatment group was higher. Conclusions Changing the cell cycle of BMHCs, decreasing the radiosensitivity of BMHCs, inhibiting the apoptosis of BMHCs and enhancing the proliferation and differentiation of BMHCs may be one of the molecular mechanisms by which GEN protects against hematopoietic damage.