论文部分内容阅读
目的:探讨泛素连接酶(Huwe1)和小清蛋白(Parvalbumin,PV)在脑性瘫痪小鼠海马组织中的表达及意义。方法:新生7 d昆明小鼠,随机分为模型组和对照组,模型组按Rice的方法手术通过结扎小鼠单侧颈总动脉并缺氧来制作脑性瘫痪模型。对照组麻醉后仅切开颈部皮肤,分离单侧颈总动脉,不结扎不剪断,然后缝合伤口,未置于缺氧环境。各组小鼠分别在术后7 d、14 d、21 d、28 d用4%多聚甲醛灌注固定、取脑、作冰冻切片,片厚30μm,应用免疫组化法检测小鼠海马组织中Huwe1和PV的表达。结果:(1)Huwe1和PV在对照组成年小鼠脑中广泛表达,在小鼠发育过程中海马各区Huwe1和PV的表达随着年龄的增加呈上升的趋势,至成年时趋于稳定;(2)模型组小鼠自术后7 d起,模型组损伤侧海马CA1、CA3、DG区Huwe1的表达均高于其对侧和对照组(P<0.05);PV的表达虽然高于其对侧,却又低于其对照组(P<0.05)。结论:Huwe1在脑性瘫痪小鼠模型损伤侧海马中表达增高可能与脑损伤后其清除异常蛋白有关。PV的低表达可能与脑缺血有关,其损伤侧一过性的高表达提示可能与脑损伤后PV缓冲胞内钙超载的能力增强有关。
Objective: To investigate the expression and significance of Huwe1 and Parvalbumin (PV) in hippocampus of cerebral palsy mice. Methods: Newborn Kunming mice on day 7 were randomly divided into model group and control group. The model group was made by the method of Rice surgery by ligating the unilateral common carotid artery and hypoxia to make cerebral palsy model. The control group was anesthetized and only the neck skin was excised. The unilateral common carotid artery was dissected, and the ligaments were not ligated without suturing. The wounds were then sutured and placed in anoxic conditions. The mice in each group were fixed with 4% paraformaldehyde at 7 d, 14 d, 21 d and 28 d after operation. The brains were harvested and frozen sections were made. The thickness of the mice was 30 μm. Immunohistochemistry Huwe1 and PV expression. Results: (1) Huwe1 and PV were widely expressed in the brains of control mice. The expressions of Huwe1 and PV in the hippocampus were increased with the increase of age in mice, 2) From the 7th day after operation, the expression of Huwe1 in CA1, CA3 and DG of the model group was higher than that of the contralateral and control groups (P <0.05). Although the expression of PV was higher than that of the control Side, but lower than the control group (P <0.05). Conclusion: The increased expression of Huwe1 in the injured side of hippocampus of cerebral palsy mouse model may be related to its clearance of abnormal protein after brain injury. The low expression of PV may be related to cerebral ischemia. The transient high expression on the injured side may be related to the increased ability of intracellular calcium overload in PV buffer after brain injury.