Hajipour Somayeh, Sarkaki Alireza, Farbood Yaghoob, Eidi Akram, Mortazavi Pejman, Valizadeh Zohreh
Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Biology, Sciences & Research Branch, Islamic Azad University, Tehran, Iran.
Basic Clin Neurosci. 2016 Apr;7(2):97-106. doi: 10.15412/J.BCN.03070203.
To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by beta-amyloid (Aβ).
Sixty-four adult male Wistar rats (300±20 g) were divided into 8 groups: 1) Control (Cont); 2) AD; 3) Sham; 4-7) AD+GA (50, 100, and 200 mg/kg for 10 days, orally) or vehicle, 8) Cont+GA100, Aβ (1μg/μL in each site) was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus (DG) were evaluated by high frequency stimulation (HFS) of perforant path (PP).
Data showed that LTP amplitude and area under curve significantly impaired in AD rats (P<0.001), while significantly improved in AD rats treated with GA (P<0.05, P<0.01).
Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of Aβ but with no effect on healthy rats.
研究没食子酸（GA）对β-淀粉样蛋白（Aβ）诱导的阿尔茨海默病（AD）动物模型海马长时程增强（LTP）及组织学变化的影响。
64只成年雄性Wistar大鼠（300±20 g）分为8组：1）对照组（Cont）；2）AD组；3）假手术组；4 - 7）AD + GA组（50、100和200 mg/kg，口服，持续10天）或溶剂对照组，8）Cont + GA100组，双侧海马注射Aβ（每个部位1μg/μL）。通过对穿通通路（PP）进行高频刺激（HFS）评估海马齿状回（DG）诱导的LTP的幅度和斜率变化。
数据显示，AD大鼠的LTP幅度和曲线下面积显著受损（P<0.001），而GA治疗的AD大鼠显著改善（P<0.05，P<0.01）。
目前的研究结果表明，GA可减少神经损伤和脑淀粉样神经病理学改变，并通过清除自由基和抑制Aβ寡聚化改善认知功能，但对健康大鼠无影响。
