Lu J, Moochhala S, Kaur C, Ling E
Defence Medical Research Institute, 18 Medical Drive, #01-06, MD2, 117597, Singapore.
Neurosci Lett. 2000 Aug 25;290(2):89-92. doi: 10.1016/s0304-3940(00)01307-0.
This study aimed to examine the temporal profile of neuronal apoptosis in the central nervous system (CNS) following closed head injury in rat. Fos immunoreactivity was detected in neuronal nuclei in the cerebral cortex at 2 h after head injury. At 4 h, Bax protein expression was elevated with a concomitant down-regulation of Bcl-2 expression. Along with this, a marked immunoexpression of p53 was also observed in these cells. Double immunolabelling study has shown the colocalization of Bax immunoreactivity with Bcl-2 and p53. In rats killed 1 day after injury, a variable number of transferase d-UTP nick-end labelling positive cells were observed. Present findings suggest that the upregulation of p53 and a shift in the ratio of Bcl-2 to Bax may contribute to neuronal apoptosis in the CNS after closed head injury.
本研究旨在检测大鼠闭合性颅脑损伤后中枢神经系统（CNS）神经元凋亡的时间变化情况。颅脑损伤后2小时，在大脑皮质神经元细胞核中检测到Fos免疫反应性。4小时时，Bax蛋白表达升高，同时Bcl-2表达下调。与此同时，在这些细胞中还观察到p53明显的免疫表达。双重免疫标记研究显示Bax免疫反应性与Bcl-2和p53共定位。在损伤后1天处死的大鼠中，观察到数量不等的末端脱氧核苷酸转移酶介导的dUTP缺口末端标记阳性细胞。目前的研究结果表明，p53的上调以及Bcl-2与Bax比值的改变可能导致闭合性颅脑损伤后中枢神经系统神经元凋亡。
