观察¹²⁵I-NGF(神经生长因子)对U251细胞DNA的损伤作用，探讨¹²⁵I-NGF的抗肿瘤作用机制。应用微核测试和单细胞电泳等方法观察U251细胞DNA的变化，Western Blotting法检测细胞蛋白水平的变化，RT-PCR法检测Cyclin B1 mRNA水平的变化，微核测试和单细胞电泳等方法观察到¹²⁵I-NGF对U251细胞DNA的损伤作用。细胞周期检测及MPM-2/PI复染实验表明¹²⁵I-NGF诱导了U251细胞G₂期阻滞。Western Blotting检测表明，¹²⁵I-NGF可能通过活化ATM和ATR途径发挥抗肿瘤作用。¹²⁵I-NGF以剂量依赖性的模式减少了U251细胞Cyclin B1蛋白表达水平，但没有改变其mRNA的表达水平。在U251细胞中，磷酸化Chk1、Chk2和Cdc25c蛋白水平提高，而p53和p21水平保持不变。阐明了¹²⁵I-NGF通过对U251细胞DNA的损伤作用活化ATM和ATR通路，使多种蛋白的表达水平发生了改变，从而发挥其抗肿瘤的作用。

The DNA-damage process of the U251 cells after being treated with ¹²⁵I-NGF is observed to show the antitumor mechanism of ¹²⁵I-NGF. The cell cycle arrest and the Western Blotting analysis were adopted to display the inherent mechanism. The micronucleus test and the single cell gel electrophoresis methods were used to observe DNA-damage changes of the U251 cells. The mechanisms involve the activation of ATM and ATR pathways by ¹²⁵I-NGF, which perhaps explains some of its anticancer activities related with nuclear transportations. In a dose-dependent manner, ¹²⁵I-NGF reduces the Cyclin B1 expression protein level rather than mRNA level in human cell lines of glioma. In U251 cells, phosphorylated Chk1, Chk2 and Cdc25c protein levels are elevated, whereas p53 and p21 levels remain unchanged. In summary, this study demonstrates that ¹²⁵I-NGF plays a role in glioma cancer growth via DNA-damage, ATM and ATR activation mechanisms and multiple proteins involved in the process.