Hwang In Koo, Yoo Ki-Yeon, Kim Duk Soo, Jeong Youn-Kab, Kim Jong Dai, Shin Hyun-Kyung, Lim Soon Sung, Yoo Ick-Dong, Kang Tae-Cheon, Kim Dong-Woo, Moon Won-Kuk, Won Moo Ho
Department of Anatomy, College of Medicine, Hallym University, Chunchon, 200-702, South Korea.
Life Sci. 2004 Sep 3;75(16):1989-2001. doi: 10.1016/j.lfs.2004.05.013.
Grape seed extract (GSE) possess cardioprotective abilities by functioning as in vivo antioxidants and by virtue of their ability to directly scavenge ROS including hydroxyl and peroxyl radicals. In the present study, we investigated the neuroprotective effects of grape seed extract (GSE) in the gerbil hippocampus after 5 min transient forebrain ischemia. Neuronal cell density in GSE-treated ischemic animals was significantly increased as compared with vehicle-treated ischemic animals 4 days after ischemic insult. In the GSE-treated groups, about 60% of pyramidal cells of the sham-operated group were stained with cresyl violet 4 days after ischemic insult. In this study, we found that GSE had neuroprotective effects on neuronal injury by inhibiting DNA damage in the CA1 region after ischemia. In vehicle-treated groups, 8-hydroxy-2'-deoxyguanosine (8-OHdG) immunoreactivity was significantly changed time-dependently, whereas the immunoreactivity in the GSE-treated group was similar to the sham-operated group. In addition, we confirmed that astrocytes and microglia did not show significant activation in the CA1 region 4 days after ischemia-reperfusion, because many CA1 pyramidal cells were not damaged. Therefore, these results suggest that GSE can protect ischemic neuronal damage by inhibiting DNA damage after transient forebrain ischemia.
葡萄籽提取物(GSE)通过作为体内抗氧化剂发挥作用,并凭借其直接清除包括羟基和过氧自由基在内的活性氧(ROS)的能力,具有心脏保护作用。在本研究中,我们研究了葡萄籽提取物(GSE)对沙土鼠前脑短暂缺血5分钟后海马体的神经保护作用。与缺血损伤4天后接受载体处理的缺血动物相比,接受GSE处理的缺血动物的神经元细胞密度显著增加。在接受GSE处理的组中,缺血损伤4天后,假手术组约60%的锥体细胞用甲酚紫染色。在本研究中,我们发现GSE通过抑制缺血后CA1区域的DNA损伤对神经元损伤具有神经保护作用。在接受载体处理的组中,8-羟基-2'-脱氧鸟苷(8-OHdG)免疫反应性随时间显著变化,而在接受GSE处理的组中,免疫反应性与假手术组相似。此外,我们证实,缺血再灌注4天后,星形胶质细胞和小胶质细胞在CA1区域未显示出明显激活,因为许多CA1锥体细胞未受损。因此,这些结果表明,GSE可以通过抑制短暂前脑缺血后的DNA损伤来保护缺血性神经元损伤。