论文部分内容阅读
目的:探讨急性酒精中毒合并中度创伤性脑损伤对大鼠海马NOS2表达和学习记忆的影响。方法:健康成年雄性SD大鼠96只,水迷宫训练3天后分为4组:生理盐水组(N组)、急性酒精中毒组(A组)、中度创伤性脑损伤组(T组)和急性酒精中毒合并中度创伤性脑损伤(AT组)。腹腔单注射25%酒精(2.5g/kg),2 h后以重物自由落体击打大鼠头部建立动物模型,存活1、3、5、7、14天。免疫组化方法检测海马CA1区NOS2表达,水迷宫检测大鼠学习记忆。结果:NOS2免疫组化染色发现各实验组阳性细胞数均高于N组。术后1天T组比AT组表达显著增高(P<0.01);术后5天AT组比T组表达增高(P<0.05);术后14天AT组比T组表达显著增高(P<0.05)。水迷宫实验测潜伏期,术后1天AT组比T组延长(P<0.05),术后3天AT组比T组缩短(P<0.05),术后14天AT组比T组显著延长(P<0.01)。结论:大鼠急性酒精中毒合并颅脑外伤后晚期,潜伏期延长,空间位置学习与记忆能力显著下降;在海马CA1区NOS2表达阳性细胞增多,为继发性脑损伤致其表达上调,是酒精急性中毒合并中度颅脑外伤预后欠佳的原因之一。
Objective: To investigate the effect of acute alcoholism combined with traumatic brain injury on NOS2 expression and learning and memory in hippocampus of rats. Methods: Ninety-six healthy adult male Sprague-Dawley rats were divided into 4 groups after 3 days of water maze training: saline group (N group), acute alcoholism group (A group), moderate traumatic brain injury group (T group) Acute alcoholism combined with moderate traumatic brain injury (AT group). Single intraperitoneal injection of 25% alcohol (2.5g / kg), 2 h after the weight of free-fall hit the head of rats to establish animal models, survival 1,3,5,7,14 days. Immunohistochemistry was used to detect the expression of NOS2 in hippocampal CA1 region and water maze to detect learning and memory in rats. Results: NOS2 immunohistochemical staining found that the number of positive cells in each experimental group were higher than the N group. The expression of AT group was higher than that of T group on day 5 postoperatively (P <0.01), and the expression of AT group was higher than that of T group on the 5th day after operation (P <0.05) 0.05). The latency of water maze test was longer in AT group than in T group (P <0.05), and the AT group was shorter than T group on the 3rd day after operation (P <0.05) P <0.01). Conclusion: In the later stage of traumatic brain injury, acute latency alcohol poisoning in rats is associated with a prolonged latency period and a significant decrease in spatial learning and memory ability. NOS2-positive cells are increased in hippocampal CA1 area and are upregulated in secondary brain injury. One of the reasons for the poor prognosis of moderate cerebral trauma combined with poisoning.