摘要
目的探讨实验性大鼠脑出血后脑组织COX-2和MAP-2的表达和两者之间的关系,及对脑组织神经元损伤的作用。方法用体重200~300 g健康的大鼠制作脑出血动物模型,将大鼠随机分为出血组和对照组;出血组分为自体血组和盐水对照组,自体血组按不同时间分为3 h、6 h、12 h、24 h、48 h、72 h、5 d、7 d、14 d、28 d、10个亚组,每组7只,盐水组为6 h组7只;正常对照组7只。用HE动态观察组织病理学改变,用免疫组织化学染色显示出血灶周围COX-2和MAP-2在脑组织内的表达。结果大鼠脑出血后脑组织COX-2于出血灶周围阳性细胞数于3 h增多,出血3 d达高峰,阳性细胞见于病变侧额顶部大脑皮质。脑出血组各时间点COX-2表达高于对照组,差异具有统计学意义(P〈0.05);MAP-2表达于出血3 h开始减少,3 d下降到最低。脑出血3 h以后,紧邻血肿周围区MAP-2阳性细胞大量消失。3 d后虽有所增加但与对照组的差异仍有统计学意义(P〈0.05)。结论COX-2主要在血肿周围的神经元表达,其高表达可能与血肿后继发性神经元损伤有关,脑出血后COX-2高表达促进了神经元的损伤,使MAP-2表达明显减少。
Objective To explore the role of COX-2 and MAP-2 in the pathological mechanism of ICH by observing the expression of MAP-2 and COX-2 in the perihematomal brain regions, and the role of them to the nerve cell. Methods Wistar rats were divided randomly into groups. Autologous hemorrhage group were divided 3 h,6 h,12 h,24 h,48 h,72 h, 5 d,7 d, 14 d,28 d, every group 7 rats. To observe the alteration of histopathology. HE and immunohistochemical technique were used to assess the pathology changed cytoskeleton impair after ICH. Results In agreement with previous reports, low levels of COX-2 observed in the brain of sham-operated rats, but the up regulation began 3h after ICH, reached a maximum at 3 d;The staining of MAP-2 decreased gradually (P 〈0.05) when compared with the control group at 3 hour after ICH and almost disappeared on the third day. Conclusion COX-2 expression in hematoma acroteric neurons,COX-2 expression in hematoma acroterie neurons contributes to ICH brain damage,the expression of MAP-2 obviously reduced.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2014年第8期695-697,共3页
Journal of Apoplexy and Nervous Diseases