Neuroprotection of catalpol in transient global ischemia in gerbils
Neuroprotection of catalpol in transient global ischemia in gerbils
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DOI：
10.1016/j.neures.2004.06.009
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发表时间：
2004-10-01
影响因子：
2.9
通讯作者：
An, LH
中科院分区：
文献类型：
--
作者：
Li, DQ;Duan, YL;An, LH
采用沙土鼠脑缺血模型，研究梓醇的神经保护作用及其机制。实验分为假手术组、梓醇组和生理盐水组。梓醇5.0mg/kg于再灌注后即刻腹腔注射，并于再灌注12、24、48、72 h重复注射。以行为学和组织学指标评价神经保护作用。在Y-迷宫中进行行为学测试，并在显微镜下计数CAI区存活神经元。此外，还采用末端脱氧核苷酸转移酶介导的UTP缺口末端标记法检测了缺血诱导的细胞凋亡。结果表明，梓醇显着减弱细胞凋亡，挽救海马CAI神经元和减少认知障碍。为了阐明梓醇的神经保护作用机制，本实验测定了皮质和海马内源性抗氧化剂和一氧化氮合酶的活性以及脂质过氧化物的含量。结果表明，梓醇显著降低了过氧化脂质的含量，提高了谷胱甘肽过氧化物酶的活性，降低了一氧化氮合酶的活性。这些结果提示梓醇是一种潜在的神经保护剂，其神经保护作用至少部分是通过促进内源性抗氧化酶活性和减少一氧化氮的生成来实现的。(C)2004年Elsevier爱尔兰有限公司和日本神经科学学会。All rights reserved.
The neuroprotection of catalpol and its mechanism was evaluated in cerebral ischemic model in gerbils. Three groups were designed as sham-operated, ischemia-treated, respectively, with catalpol and saline. Catalpol was injected intraperitoneally immediately after reperfusion and repeatedly at 12, 24, 48 and 72h with the dose of 5.0 mg/kg. The neuroprotection was estimated by the indexes of behavior and histology. Behavioral testing was per-formed in Y-maze and the survival neurons in CAI subfield were counted under a microscope after behavioral testing. In addition, apoptosis induced by ischemia was also examined by using the terminal deoxynucleotidyl transferase-mediated UTP nick end labeling method. It was shown that catalpol significantly attenuated apoptosis, rescued hippocampal CAI neurons and reduced cognitive impairment. In order to make clear the mechanism of catalpol's neuroprotection, the activities of endogenous antioxidants and nitric oxide synthase together with the content of lipid peroxide in cortex and hippocampus were assayed. The results proved that catalpol significantly reduced the content of lipid peroxide, increased the activity of glutathione peroxidase and decreased the activity of nitric oxide synthase. All these suggested that catalpol was a potential neuroprotective agent and its neuroprotective effects were achieved at least partly by promoting endogenous antioxidant enzymatic activities and reducing the formation of nitric oxide. (C) 2004 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.