摘要
目的研究慢性脑缺血大鼠海马聚腺苷二磷酸核糖聚合酶(PARP)的表达,并探讨阿魏酸钠在慢性脑缺血所致的氧化应激性损伤中的作用。方法28只成年大鼠用于实验,10只采用双侧颈总动脉结扎制备大鼠慢性脑缺血模型,10只在颈总动脉结扎后给立即予阿魏酸钠腹腔注射,另8只为假手术组。2月后取大鼠海马,采用硫代巴比妥酸法检测丙二醛(MDA)含量,用免疫印迹的方法检测PARP蛋白的表达量。结果慢性脑缺血大鼠海马MDA及PARP蛋白含量明显增多,而经阿魏酸钠治疗后,MDA含量下降,PARP表达下调。结论慢性脑缺血可诱导内源性氧化应激使自由基增多,产生脂质过氧化损伤作用,并导致DNA链的断裂,激活PARP的表达;阿魏酸钠可减少MDA和PARP的生成,在慢性脑缺血氧化应激中起保护作用。
Objective We examined the effect of chronic cerebral hypoperfusion on the the expression of Poly(ADP-ribose) Polymerase(PARP) in rat hippocampus and studied the role of sodium ferulate in oxidative stress during chronic cerebral hypoperfusion. Methods Bilateral common carotid arteries were permanently double ligated in 10 Wistar rats. 10 rats were administered sodium ferulate after chronic cerebral ischemic immediately. Other 8 rats were sham-operated group. The contents of malondialdehyde (MDA)in the hippocampus were detected. The levels of PARP protein was measured by Western blot. Results The content of MDA after chronic cerebral hypoperfusion increased significantly. The levels of PARP were higher than that of the sham-operated group. In sodium ferulate-treated rats,the level of MDA and PARP were lower than that of the group of 2-VO. Conclusion Chronic cerebral hypoperfusion can induced oxidative stress and increased reactive oxygen hydroxyl ions,which can produce lipidperoxide,induce DNA damage,resulte activation of poly(ADP-ribose) polymerase. Sodium ferulate can protect brain against oxidative damage after chronic cerebral ischemia.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2005年第3期213-215,共3页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金(301160719)
关键词
慢性脑缺血
氧化应激
PARP
MDA
阿魏酸钠
Chronic cerebral hypoperfusion
Oxidative stress
PARP
MDA
Sodium ferulater
