Li Dan-Qing, Duan Yan-Long, Bao Yong-Ming, Liu Chui-Ping, Liu Ying, An Li-Jia
Department of Bioengineering, Environment and Life School, Dalian University of Technology, No 2 Linggong Road, Dalian, Liaoning 116023, PR China.
Neurosci Res. 2004 Oct;50(2):169-77. doi: 10.1016/j.neures.2004.06.009.
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 72 h with the dose of 5.0 mg/kg. The neuroprotection was estimated by the indexes of behavior and histology. Behavioral testing was performed in Y-maze and the survival neurons in CA1 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 CA1 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.
在沙土鼠脑缺血模型中评估了梓醇的神经保护作用及其机制。设计了三组，分别为假手术组、梓醇治疗的缺血组和生理盐水治疗的缺血组。再灌注后立即腹腔注射梓醇，剂量为5.0mg/kg，并在12、24、48和72小时重复注射。通过行为学和组织学指标评估神经保护作用。在Y迷宫中进行行为测试，行为测试后在显微镜下计数CA1亚区的存活神经元。此外，还使用末端脱氧核苷酸转移酶介导的UTP缺口末端标记法检测缺血诱导的细胞凋亡。结果表明，梓醇可显著减轻细胞凋亡，挽救海马CA1神经元并减轻认知障碍。为了明确梓醇神经保护作用的机制，检测了皮质和海马中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。结果证明，梓醇可显著降低脂质过氧化物含量，提高谷胱甘肽过氧化物酶活性，降低一氧化氮合酶活性。所有这些表明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形成来实现的。
