大鼠C6脑胶质瘤X刀治疗后细胞周期的改变及相关蛋白的表达

The changes of cell cycle and the expression of p16, Cyclin D1 and Cdk4 of C6 rat glioma cell after X-radiation

目的通过观察大鼠C6脑胶质瘤模型经X射线照射后细胞周期的改变及相关蛋白P16、CyclinD1和Cdk4的表达,探讨辐射对肿瘤的杀伤机制。方法建立大鼠C6脑胶质瘤颅内接种模型,通过免疫组化法检测其经X射线照射后P16、CyclinD1和Cdk4的表达情况及应用流式细胞仪检测其细胞周期的变化。结果肿瘤经X射线照射后,胶质瘤细胞出现G1百分数增多,S期细胞百分数减少,诱导发生了G1阻滞。P16蛋白表达量显著增高,Cyclin D1和Cdk4表达显著下降,与对照组相比具有显著性(P<0.05);且这种变化具有时程效应,即P16蛋白在24h时表达最高,CyclinD1、Cdk4在48h时表达最低。结论辐射可诱导细胞发生G1阻滞,P16、CyclinD1和Cdk4在辐射诱导的G1阻滞中起着重要的作用。

Objective To explore the mechanism of killing tumor cells by observing the changes of cell cycle and the expression of p16、Cyclin D1 and Cdk4 of C6 rat glioma cell after X-radiation.Methods After X-radiation in the C6 rat glioma models, the immunohistochemistry technique was employed to detect P16、Cyclin D1 and Cdk4 protein expression. Flow cytometry was employed to observe the changes of cell cycle.Results Radiotherapy can induce G1-phase arrest. P16 protein expression in the treatment group is higher than that in control group(P<0.05) and is highest at 24h after X-radiation, but the Cyclin D1、Cdk4 protein expression in the treatment group is lower than that in control group(P<0.05) and is lowest at 48h after X-radiation.Conclusion X-radiation can induce G1-phase arrest. P16、Cyclin D1 and Cdk4 play an important role in radiation-induced cell cycle arrest.