摘要
目的:研究盐酸戊乙奎醚对感染性脑水肿保护作用的机制。方法:采用左颈内动脉注射脂多糖复制大鼠感染性脑水肿模型,将84只雄性SD大鼠随机分为对照组(C组)、水肿组(I组)、盐酸戊乙奎醚治疗组(P组)。检测6 h、12 h、24 h、48 h时各组大鼠脑组织含水量、病理形态;脑组织SOD活性、MDA含量;免疫组化法及RT-PCR法检测AQP4蛋白分布与AQP4mRNA含量。结果:(1)与C组相比,I组、P组脑含水量、MDA含量均升高,同时SOD活性、AQP4蛋白、AQP4mRNA表达均减少(P<0.01)。与对应时间点P组相比,I组脑含水量、MDA含量均升高,同时SOD活性、AQP4蛋白、AQP4mRNA表达均减少,于24 h达高峰,48 h仍在较高水平(P<0.01)。(2)脑组织光镜检查:I组大鼠脑组织损伤严重,P组损伤明显减轻。结论:盐酸戊乙奎醚能在一定程度上可减轻感染所致的脑组织损伤,上调AQP4表达,对脑水肿有一定治疗作用,其机制可能与抗氧化作用有关。
Objective: To investigate the effects of penehyclidine on endotoxin-induced brain edema and its possible mechanism. Methods: The infection brain edema model was induced by LPS 150 μg injection in the internal carotid artery. 84 male SD rats were randomly divided into 3 groups (n = 28 ) :control group (group C ) , edema group (group I) , penehyclidine group (group P). The animals were decapitated at 6 h,12 h,24 h and 48h after operation (n =7 at each time point in each group). The brain water content, SOD activity, MDA content is measured, and AQP4 protein is detected by immunohistoehemistry, as well as AQP4mRNA by RT-PCR. Results: 1. Compared with the group C, the brain water content, MDA content was increased ( P 〈 0.01 ) ; SOD activity, AQP4 protein, AQP4mRNA expression reduction at the same time point in group I and group P ( P 〈 0. 01 ) ; compared with the Group P, the brain water content, MDA content was increased ( P 〈 0.01 ) ;SOD activity, AQP4 protein, AQP4mRNA expression reduction at the same time point in group I( P 〈 0. 01 ), and reached the peak at 24 h, remained at a relatively high level in 48 h. 2. Light and electron microscopy: the brain injury seriously in group I, the slightly attenuated in group P. Conclusion:Penehyelidine can reduce blood brain barrier injury, increase AQP4 expression, and alleviate brain edema, to a certain extent of the treatment, which may be related to the antioxidant effects.
出处
《世界科技研究与发展》
CSCD
2009年第2期357-360,共4页
World Sci-Tech R&D
基金
重庆市科委自然基金面上项目(CSTC
2007BB5279)