辐射对RANKL诱导RAW264.7细胞向破骨细胞分化中CBFα1表达水平的影响

Effect of radiation on CBFα1 expression in RANKL-induced osteoclast differentiation of RAW264.7 cells

为了研究辐射对于破骨细胞中Notch通路的影响,进一步了解辐射诱发骨损伤的机理,本研究采用核因子κB受体活化因子配体(Receptor activator of nuclear Factor-B Ligand,RANKL)诱导RAW264.7细胞系生成的破骨细胞,经2 Gy 137Csγ射线照射后应用实时定量聚合酶链反应(Real-time polymerase chain reaction,Real-time PCR)方法,检测其Notch通路重要靶位启动子C结合因子α1(C Promoter-Binding Factorα1,CBFα1)表达的变化情况。实验结果表明,在2 Gy 137Csγ射线照射后,CBFα1在RANKL作用下生成的破骨细胞中表达明显增高。辐射诱发的Notch通路中CBFα1表达增高,可能是由于辐射增强了Notch通路对破骨细胞分化的促进作用,增加了破骨细胞的数量,增强了其活性,从而导致骨损伤、骨质疏松、甚至骨折的发病率增高。

In order to investigate the changes of the Notch signaling pathway in osteoclast after radiation the mechanism radiation-induced bone loss,the gene expression of CBFα1,the important signal molecular in Notch sig-naling pathway was measured by real-time PCR,respectively.The osteoclast was obtained by RANKL-dependent differentiation in the RAW264.7 cell line.It was found that the 2 Gy 137Cs γ-rays enhanced the CBFα1 expression in RANKL-induced osteoclasts.Taken together,the higher expression of CBFα1 might reinforce the effect of promoting osteoclastogenesis by Notch signaling pathway,increase both of the number and activity of osteoclasts while the bone loss,osteoporosis and fracture occur.