Volume 11, Issue 4 (10-2007)                   ibj 2007, 11(4): 237-243 | Back to browse issues page

DOI: -
PMID: 18392085

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Progressive cognitive decline is one of the hallmark symptoms of Alzheimer’s disease (AD) which can be modeled by β-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 β-amyloid-induced memory and coordination impairment in rats. Methods: 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 µl of sterile saline or water containing 2 nmol/µl β-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. Results: We found that β-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. Conclusion: We concluded that EGCG can be effective in restoring β-amyloid-induced behavioral derangements in rats regarding coordination and memory abilities.
Type of Study: Full Length | Subject: Related Fields