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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 study the effect of radiation on Notch pathway in osteoclasts, and to further understand the mechanism of radiation-induced bone damage, we used RAW264.7 (RANKL) to induce RAW264.7 The cell line generated osteoclasts were irradiated with 2 Gy of 137Csγ ray and then detected by Real-time PCR (Real-time PCR) (C Promoter-Binding Factorα1, CBFα1) expression changes. The experimental results showed that the expression of CBFα1 in osteoclasts generated by RANKL significantly increased after irradiation with 2 Gy 137Csγ-rays. Increased expression of CBFα1 in the radiation-induced Notch pathway may be due to the radiation-induced enhancement of osteoclast differentiation by the Notch pathway, increasing the number of osteoclasts and increasing their activity, leading to bone damage, osteoporosis, and even The incidence of fractures increased.