Rasoolijazi Homa, Joghataie Mohammad Taghi, Roghani Mehrdad, Nobakht Maliheh
Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Department of Physiology, School of Medicine, Shahed University, Tehran, Iran
Iran Biomed J. 2007 Oct;11(4):237-43.
Progressive cognitive decline is one of the hallmark symptoms of Alzheimer's disease (AD) which can be modeled by beta-amyloid injection into specific regions of brain. Since epigallocatechin-3-gallate (EGCG) is a potent antioxidant agent which its role against oxidative stress and inflammation has been shown in prior studies, we tried to determine whether EGCG administration protects against beta-amyloid-induced memory and coordination impairment in rats.
Animals (male Wistar rats) were divided into four groups: sham operated, EGCG-pretreated sham operated (sham+EGCG), untreated lesion (lesion), and EGCG-pretreated lesion (lesion+EGCG). Animals in lesion, lesion+EGCG, and sham+EGCG groups received sterile saline or saline plus EGCG (10 mg/kg) intraperitoneally one day pre-surgery and every other day for three weeks. The lesion was induced one day after EGCG pretreatment by injection of 4 microl of sterile saline or water containing 2 nmol/microl beta-amyloid (1-40) into the hippocampal fissure. For behavioral analysis, psychomotor coordination (PMC) index and spontaneous alternation behavior were assessed using Rota-rod Treadmill and Y-maze, respectively at the third week post-lesion.
We found that beta-amyloid (1-40) injection into hippocampus can decrease these behavioral indexes in lesion group in comparison with sham group which is similar to behavioral changes in AD. On the other hand, pretreatment with EGCG can improve the PMC index and spatial Y-maze alternation in the lesion+EGCG group in comparison with lesion group.
We concluded that EGCG can be effective in restoring beta-amyloid-induced behavioral derangements in rats regarding coordination and memory abilities.
进行性认知衰退是阿尔茨海默病(AD)的标志性症状之一,可通过向大脑特定区域注射β-淀粉样蛋白来模拟。由于表没食子儿茶素-3-没食子酸酯(EGCG)是一种强效抗氧化剂,先前的研究已表明其在对抗氧化应激和炎症方面的作用,我们试图确定给予EGCG是否能预防β-淀粉样蛋白诱导的大鼠记忆和协调能力损害。
将动物(雄性Wistar大鼠)分为四组:假手术组、EGCG预处理假手术组(假手术+EGCG)、未处理损伤组(损伤组)和EGCG预处理损伤组(损伤+EGCG)。损伤组、损伤+EGCG组和假手术+EGCG组的动物在手术前一天腹腔注射无菌生理盐水或生理盐水加EGCG(10mg/kg),此后每隔一天注射一次,共三周。在EGCG预处理一天后,通过向海马裂注射4微升无菌生理盐水或含2nmol/微升β-淀粉样蛋白(1-40)的水来诱导损伤。为进行行为分析,在损伤后第三周分别使用转棒式跑步机和Y迷宫评估精神运动协调(PMC)指数和自发交替行为。
我们发现,与假手术组相比,向海马注射β-淀粉样蛋白(1-40)可降低损伤组的这些行为指标,这与AD中的行为变化相似。另一方面,与损伤组相比,EGCG预处理可改善损伤+EGCG组的PMC指数和空间Y迷宫交替行为。
我们得出结论,EGCG在恢复β-淀粉样蛋白诱导的大鼠协调和记忆能力行为紊乱方面可能有效。