Effects of ethanol extracts of scorpion on hippocampal apoptosis and caspase-3 expression in lithium chloride-pilocarpine-induced status epilepticus rats
Effects of ethanol extracts of scorpion on hippocampal apoptosis and caspase-3 expression in lithium chloride-pilocarpine-induced status epilepticus rats作者机构:Department of Neurology Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital Chengdu 610072 Sichuan Province China
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2010年第5卷第2期
页 面:118-125页
核心收录:
学科分类:10[医学]
基 金:the National Natural Science Foundation of China,No.30740035 the Tackle Key Program of Sichuan Province,No.05SG1672
主 题:ethanol extracts of scorpion apoptosis terminal dUTP nick-end labeling caspase-3 model of status epilepticus lithium chloride-pilocarpine brain injury neural regeneration
摘 要:BACKGROUND: Previous studies have demonstrated that scorpion venom in the scorpion can inhibit epilepsy and apoptosis. However, it remains unclear whether ethanol extracts of scorpion (EES) exhibit similar effects. OBJECTIVE: To investigate the effects of EES on hippocampal apoptosis and caspase-3 expression, and to compare the effects on sodium valproate (positive control drug) in a rat model of status epilepticus induced by lithium chloride-pilocarpine. DESIGN, TIME AND SETTING: This randomized, controlled study was conducted at the Drug Research and Development Center, Kanghong Pharmaceuticals Group, and the Department of Pathology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, China from May 2007 to April 2008. MATERIALS: EES were prepared by Huashen Pharmaceutical, China. Sodium valproate (Hunan Xiangzhong Pharmaceutical, China) and lithium chloride-pilocarpine (Sigma, USA) were also used in the present study. METHODS: From a total of 156 rats, six served as normal controls. The remaining rats were intraperitoneally injected with lithium chloride-pilocarpine to establish status epileptlcus models, and then assigned to five groups (n = 30, respectively). Animals in each group were administered drugs at 15 minutes after epileptic seizure by gavage, i.e. in the normal control and model groups, rats were treated with 1 mL/0.1 kg saline. The sodium valproate group was administered 120 mg/kg/d sodium valproate. The low-, moderate-, and high-dose EES groups received treatments of 290, 580 and 1 160 mg/kg/d EES. The dispensed concentration was 1 mL/0.1 kg. Rat seizure behavior was observed. If status epilepticus did not terminated after 1 hour, the rats were intraperitoneally administered atropine (1 mg/kg) and diazepam (10 mg/kg) to terminate seizure. These rats were continuously observed for 6 hours to ensure seizure termination. Then rats were treated with the above-mentioned drugs at 8:00 am each day until sacrifice, which took place 4