文献类型：期刊文献

中文题名：东亚钳蝎有效部位抗癫痫作用及其对癫痫小鼠海马细胞抗氧化能力的影响

英文题名：Antiepilepsy of the active fraction extracted from Buthus martensic Karsch and its effect on the oxidation resisting level in hippocampus cells

作者：宋利琼[1];林强[2];刘杨平[2];任超[2];黄迎春[2]

第一作者：宋利琼

机构：[1]三峡大学医学院生物病原部;[2]北京联合大学生物化学工程学院

第一机构：三峡大学医学院生物病原部,宜昌市443000

年份：2009

卷号：25

期号：3

起止页码：43-45

中文期刊名：中药药理与临床

外文期刊名：Pharmacology and Clinics of Chinese Materia Medica

收录：北大核心:【北大核心2008】；CSCD:【CSCD_E2011_2012】；

基金：北京市教育委员会科技发展计划面上项目(KM200711417008);三峡大学青年基金项目(KJA0304)

语种：中文

中文关键词：东亚钳蝎;戊四氮;癫痫;超氧化物歧化酶;丙二醛

外文关键词：Buthus martensic Karsch; epilepsy; superoxide dismute; malondiadehyde

摘要：目的:研究的抗癫痫作用及其机理。方法:腹腔注射PTZ观察癫痫发作等级,之后各组连续7天分别灌胃丙戊酸钠组(VPA)及不同剂量东亚钳蝎有效部位(AFBmK),于末次灌胃4h后再次注射PTZ并观察发作等级,断头分离海马,检测小鼠海马内超氧化物歧化酶(SOD)、丙二醛(MDA)的变化。结果:AFBmK显著降低发作等级,提高SOD的活性,降低MDA的含量。结论:AFBmK能够治疗PTZ诱发的小鼠癫痫,其作用机理之一为提高小鼠海马SOD活性,或直接清除自由基,增强了海马细胞的抗氧化水平,降低了过氧化作用。
To study molecular mechanism of antiepilepsy of the active fraction extracted from Buthus martensic Karsch. Methods ： 60 male mice were divided into 6 groups randomly including the nomal control（NC） , PTZ-indueed（PTZ） , vaproate sodium（ VAP, positive control drug） treating and AFBmK（L） , AFBmK（ M）, AFBmK（H） treating groups. Except NC group, the other groups were injected with pentylenetetrazol （PTZ） by abdominocentesis. The spasm grades of epilepsy were observed. Then all of groups were given VPA and various dosages of AFBmK by gastrogavage for 7 days. After four hours of last gastrogavage and except NC group, the other groups were injected with pentylenetetrazol （PTZ） by abdominocentesis ,then the spasm grades of epilepsy were observed, mice were decollated in oder to separtate hippocampus. Changes of superoxide dismutase （SOD） activities and malondiadehyde （MDA） contents were detected. Results： AFBmK （L） evidently decresed the spasm grades of PTZ-induced epileptic mice （P 〈 0.01）. AFBmK（M） and AFBmK（H） excessively decresed the spasm grades of epileptic mice （ P 〈 0.001 ）. AFBmK （ L）, AFBmK （M） and AFBmK （H） all excessively increased the activities of SOD （ P 〈 0.001 ） and decresed the contents of MDA（ P 〈 0. 001 ）. Conclusion ： AFBmK had a strong therapy effect on PTZ-induced epileptic mice. The reason may be that AFBmK increased the activities of SOD, so that oxidation resisting level is enhanced, the cell overoxidation is decreased in hippocampus cells, and therapy epileptic.