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背景:创伤性脑损伤神经细胞存在着细胞凋亡。有研究证实Bcl-2基因参与人脑挫裂伤后神经细胞的凋亡。聚二磷酸腺苷核糖多聚酶(polyadeno-sinediphosphateribosepolymerase,PARP)是细胞凋亡的一个重要标志。目的:通过对大鼠创伤性脑损伤后PARP降解与DNA片段化的时序关系的研究,了解大鼠创伤性脑损伤后神经细胞凋亡的变化进程。设计:随机对照的实验研究。单位:白求恩军医学院和白求恩国际和平医院。材料:选择Wister大鼠30只,随机分为假手术组5只和脑损伤组25只。方法:采用Feeney等的落体撞击法造成左顶叶局限性脑挫裂伤,落体致伤冲击力为500g·cm(50g,10cm),分别于损伤后2,6,12,24,48h处死取样。分别采用末端标记法测定DNA片段化,免疫组化法检测PARP降解。光镜下观察阳性细胞所在部位及形态,苏木精-伊红染色作对照观察。主要观察指标:损伤后脑皮质PARP降解与DNA片段化阳性细胞数。结果:脑损伤后2h开始出现PARP降解,主要集中于损伤灶边缘部位。6h开始出现DNA片段化,最高密度均集中于损伤灶边缘部位,随时间推移,损伤灶深部区可见散在单个阳性细胞。其中PARP降解高峰出现在12～24h(48～46个阳性细胞/切片,t=-34.434,-41.196,P<0.001),DNA片段化出现高峰在24～48h(60～56个阳性细胞/切片,t=-39.430,-61.933,P<0
BACKGROUND: Traumatic brain injury has neuronal apoptosis. Studies have confirmed that Bcl-2 gene is involved in neuronal apoptosis after contusion and laceration in human. Polyadeno-sipiphosphateribose polymerase (PARP) is an important marker of apoptosis. OBJECTIVE: To study the relationship between PARP degradation and DNA fragmentation after traumatic brain injury in rats, and to understand the process of neuronal apoptosis after traumatic brain injury in rats. Design: Randomized controlled experimental study. Units: Bethune Military Medical College and Bethune International Peace Hospital. MATERIALS: Thirty Wister rats were randomly divided into sham-operated group (n = 5) and brain injury group (n = 25). Methods: The tethering injury of the left parietal lobe was induced by the falling body impacting method of Feeney et al. The impact force of falling body was 500g · cm (50g, 10cm), and sacrificed at 2, 6, 12, 24, 48h after injury . DNA fragmentation was determined by end-labeling method, and the degradation of PARP was detected by immunohistochemistry. Observed by light microscope, the location of positive cells and morphology, hematoxylin-eosin staining control. MAIN OUTCOME MEASURES: Degradation of PARP and DNA fragmented positive cells in cerebral cortex after injury. Results: The degradation of PARP started 2h after brain injury, which mainly focused on the margins of lesions. 6h began to appear DNA fragmentation, the highest density are concentrated in the edge of the lesion, with the passage of time, scattered lesions in the deep area can be seen scattered in a single positive cells. The peak of PARP degradation appeared at 12-24 h (48-46 positive cells / section, t = -34.434, -41.196, P <0.001), and the peak of DNA fragmentation appeared at 24-48 h (60- 56 positive cells / section , t = -39.430, -61.933, P <0