论文部分内容阅读
背景:细胞水肿与水的转运有关,水的转运与水通道蛋白(aquaporin、AQP)密切相关,研究脑水肿与水通道蛋白关系,会为进一步阐述脑水肿的发病机制奠定基础。目的:探讨缺血性脑水肿后AQP-4的变化,研究脑水肿的发病机制。设计:完全随机对照实验研究。地点和对象:实验地点为吉林大学第一医院。选用Wistar雄性大鼠42只,体质量250～300g,鼠龄3～4月,按缺血时间随机分为6h,1,3,5,7,14d及假手术组,每组6只。干预:参考Longa等方法建立大鼠大脑缺血模型,苏木精-伊红染色观察组织病理学改变,应用免疫组化染色检测脑组织中AQP-4的变化。主要观察指标:缺血组及假手术组脑组织病理表现及AQP-4染色阳性细胞数。结果:在缺血6h组主要表现为:神经元固缩,有轻度水肿。缺血1d组和3d组,神经元出现胞核崩解,胞浆淡染,同时出现明显的水肿,有的神经元只剩下淡红色的印记。AQP-4在缺血组织表达增强,缺血6h即增强犤(18.03±1.51)个/视野犦,1d时为犤(23.05±2.01)个/视野犦,3d达高峰犤(38.14±2.12)个/视野犦,5d时为犤(21.75±1.80)个/视野犦,与假手术组比较,差异有显著性意义(t=14.88～29.32,P<0.01),7d恢复正常犤(9.03±1.25)个/视野犦。结论:AQP-4是影响缺血性脑水肿的重要因素。
BACKGROUND: Cell edema is associated with water transport and water transport is closely related to aquaporin (AQP). Studying the relationship between cerebral edema and aquaporin may provide the basis for further elucidating the pathogenesis of cerebral edema. Objective: To investigate the changes of AQP-4 after ischemic cerebral edema and to study the pathogenesis of cerebral edema. Design: Complete randomized controlled experimental study. Location and object: The experimental site for the First Hospital of Jilin University. Forty - two Wistar male rats weighing 250-300g were randomly divided into 6h, 1,3,5,7 and 14 days and sham operation group, 6 rats in each group. Intervention: The rat model of cerebral ischemia was established by reference to Longa et al. The changes of histopathology were observed by hematoxylin-eosin staining. The changes of AQP-4 in brain tissue were detected by immunohistochemical staining. MAIN OUTCOME MEASURES: Cerebral histopathology and number of AQP-4 positive cells in ischemic group and sham operation group. Results: The 6h ischemia group mainly manifested as: neuronal shrinkage, mild edema. Ischemia 1d group and 3d group, neurons appear nucleus disintegration, light cytoplasm, while significant edema, and some neurons only pink mark. The expression of AQP-4 was enhanced in ischemic tissue and increased (18.03 ± 1.51) / visual field at 6h after ischemia, 犤 (23.05 ± 2.01) / visual fields at 1d and 38.14 ± 2.12 / (21.5 ± 1.80) / visual field at 5 days, the difference was significant (t = 14.88-29.32, P <0.01), and returned to normal at 7 days (9.03 ± 1.25) A / vision 犦. Conclusion: AQP-4 is an important factor affecting ischemic cerebral edema.