60Coγ射线诱导的新生大鼠大脑皮质神经细胞凋亡

目的 采用电离辐射诱导的新生大鼠大脑皮质神经细胞损伤模型,探讨电离辐射诱导发育脑神经细胞死亡的特征和机制。方法 新生大鼠接受单次2.0 Gyγ射线照射后,采用DNA凝胶电泳、TUNEL和HE染色鉴定大脑皮质神经细胞死亡的类型和时程变化特点;应用免疫组织化学方法研究p53和iNOS在细胞死亡过程中的可能作用。结果 DNA凝胶电泳、TUNEL和HE染色表明,2.0 Gyγ射线照射可诱导新生大鼠大脑皮质神经细胞凋亡。大脑皮质各区域凋亡指数于照射后4 h开始增高,至12 h达到峰值;照射后相同时间点各皮质区域凋亡指数比较,新皮质最高,海马次之,旧皮质最低;P53和iNOS免疫阳性细胞计数定量结果显示,照射后相同时间点各皮质区域P53和iNOS免疫阳性细胞数差异无统计学意义。结论 2.0 Gyγ射线照射诱导了新生大鼠大脑皮质神经细胞凋亡;不同皮质区域的神经细胞对电离照射引起的损伤反应是相似的,但不同皮质区域的神经细胞凋亡存在差异。

Apoptosis of neural cells in the neonatal rat cerebral cortex induced by 60Co Gamma Ray

Objective To identify the cell death type and investigate the potential mechanism of ionizing radiation-induced neural cell death in the neonatal rat cerebral cortex.Methods The neonatal Wistar rats were given a single dose of 2.0 Gy γ-irradiation.The cell death type and characterization in cerebral cortex were identified using DNA electrophoresis,TUNEL and HE staining.The P53-and iNOS-positive cells were analyzed quantitatively using immunohistochemistry.Results The DNA and morphological characterization of death cells indicated that 2.0 Gy γ-irradiation induced apoptosis of the neural cells in neonatal rat cerebral cortex.The apoptosis indices in different cortex regions were significantly increased 4 h after irradiation,and reached the peak value at 12 h post-irradiation.The apoptosis index of neoconex was much higher than that of hippocampus(archicortex)and paleocortex,while paleocortex had lower apoptosis index than hippocampus.The quantitative immunohistoehemistry suggested that the numbers of P53 and iNOS-positive cells were not different between these three cortex regions at the same time-point after irradiation.Conclusion 2.0 Gy γ-rays induced apoptosis of the neural cells in neonatal rat cerebral codex.The response of cells to the damage effects of ionizing radiation was similar in different cortex regions;however,the apoptosis indices were different significantly.These findings imply that the developing phase or type of neural cells may play a pivotal role in the apoptosis process induced by ionizing radiation.