Protective effects of Choto-san and hooks and stems of Uncaria sinensis against delayed neuronal death after transient forebrain ischemia in gerbil
Protective effects of Choto-san and hooks and stems of Uncaria sinensis against delayed neuronal death after transient forebrain ischemia in gerbil
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DOI：
10.1016/j.phymed.2003.04.001
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发表时间：
2004-09-01
期刊：
影响因子：
7.9
通讯作者：
Terasawa, K
中科院分区：
文献类型：
--
作者：
Yokoyama, K;Shimada, Y;Terasawa, K
在此之前，我们揭示了钩藤(Uncaria sinsis(Oliv.)HAVIL.是一种药用植物，含有赤参，在体外具有神经保护作用。在本研究中，为了阐明它们在体内的作用，我们观察了沙土鼠口服赤参提取物(CSE)或中华绒毛提取物(USE)是否能减少沙土鼠脑缺血/再灌流(I/RP)后迟发性神经元死亡。采用双侧颈总动脉结扎4min造成沙土鼠短暂性前脑缺血模型，将1.0%和3.0%CSE或USE两个剂量(1.0%和3.0%)溶解于饮用水中，从I/RP前7天至I/RP后7天随意给药。结果发现，1.0%和3.0%CSE处理显著减少了I/RP后7d大鼠海马CA1区锥体细胞的死亡。在I/RP后7天，3%的Use处理也显著抑制锥体细胞的死亡。1.0%CSE处理组和3.0%Use处理组大鼠缺血/再灌流后7d脑组织匀浆清除超氧阴离子和羟基自由基活性均显著高于对照组。此外，1.0%CSE组和3.0%Use组I/RP后48h脑组织匀浆中脂质过氧化水平和NO2-/NO3-水平均显著低于对照组。这些结果表明，口服CSE或USE可通过减少对神经元的氧化损伤而对短暂性缺血诱导的迟发性神经元死亡起到保护作用。(C)2004年爱思唯尔股份有限公司。版权所有。
Previously, we revealed that Choto-san (Diao-teng-san in Chinese), a Kampo formula, is effective on vascular dementia clinically, and the hooks and stems of Uncaria sinensis (OLIV.) HAVIL., a medicinal plant comprising Choto-san, has a neuroprotective effect in vitro. In the present study, for the purpose of clarifying their effects in vivo, we investigated whether the oral administration of Choto-san extract (CSE) or U. sinensis extract (USE) reduces delayed neuronal death following ischemia/reperfusion (i/rp) in gerbils. Transient forebrain ischemia was induced by bilateral carotid artery occlusion for 4min, and two doses (1.0% and 3.0%) of CSE or USE were dissolved in drinking water and provided to the gerbils ad libitum from 7 days prior to i/rp until 7 days after i/rp. It was found that 1.0% and 3.0% CSE treatments significantly reduced pyramidal cell death in the hippocampal CAI region at 7 days post i/rp. Three percent USE treatment also inhibited pyramidal cell death significantly at 7 days after i/rp. Superoxide anion and hydroxyl radical scavenging activities of the homogenized hippocampus at 7 days after i/rp in the 1.0% CSE- and 3.0% USE-treated groups were significantly enhanced compared to those of control. Further, lipid peroxide and NO2-/NO3- levels of the homogenized hippocampus at 48 h after i/rp in the 1.0% CSE- and 3.0% USE-treated groups were significantly lower than those of control. These results suggest that the oral administration of CSE or USE provides a protective effect against transient ischemia-induced delayed neuronal death by reducing oxidative damage to neurons. (C) 2004 Elsevier GmbH. All rights reserved.