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作 者:谢涛[1] 和学欣 张卓 毛卓锋[1] 王晓鹏[1] Xie Tao;He Xuexin;Zhang Zhuo;Mao Zhuofeng;Wang Xiaopeng(Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)
机构地区:[1]河北医科大学第二医院神经内科,石家庄050000 [2]石家庄市中医院康复科
出 处:《脑与神经疾病杂志》2021年第5期270-273,共4页Journal of Brain and Nervous Diseases
基 金:国家自然基金项目(81671292)。
摘 要:目的探讨表没食子儿茶素没食子酸脂(epigallocatechin-3-gallate,EGCG)对戊四氮(pentylenetetrazole,PTZ)致痫大鼠行为学影响及其作用机制。方法采用戊四氮致痫癫痫大鼠模型,将7~8w龄清洁级健康雄性Sprague-Dawley(SD)大鼠随机分为五组:模型组(PTZ组);正常对照组(CON组);25mg·kg^(-1) EGCG+PTZ组;50mg·kg^(-1) EGCG+PTZ组;50mg·kg^(-1) EGCG组。行为学分级标准依据Racine分级,同时观察肌阵挛潜伏期、癫痫大发作潜伏期和癫痫大发作持续时间。给药结束后24h,各组大鼠断头处死,测定全脑还原型谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)含量。结果(1)EGCG干预可有效降低癫痫大鼠发作级别和癫痫大发作持续时间、延长肌震挛潜伏期及癫痫大发作潜伏期;(2)EGCG干预升高了癫痫大鼠脑内GSH水平;同时降低了MDA水平。结论EGCG可以有效抑制戊四氮诱导的癫痫发作,其抗癫痫作用可能是通过抗氧化作用来实现的。Objective To investigate the effect of epigallocatechin-3-gallate(EGCG)on the behavior of epileptic rats induced by pentylenetetrazole and its mechanism.Method Epilepsy rat model induced by pentylenetetrazole was used.Healthy male Sprague-Dawley(SD)rats aged 7-8 weeks were separated into five groups randomly:model group(PTZ group);control group(CON group);25 mg·kg^(-1)EGCG+PTZ group;50 mg·kg^(-1)EGCG+PTZ group;50 mg·kg^(-1)EGCG group.Behavioral classification was based on Racine classification.The latency to myoclonic jerks and the generalized tonic clonic seizures(GTCS)as well as duration of GTCS were also recorded.24 hours after the end of administration,the rats in each group were decapitated and killed,and the contents of GSH and MDA in the whole brain were determined.Results(1)EGCG intervention can effectively reduce the seizure grade and duration of GTCS,prolong the latency to myoclonic jerks and the GTCS;(2)After EGCG intervention,GSH level in epileptic rats was increased,while MDA level was reduced.Conclusion EGCG can effectively inhibit pentylenetetrazole-induced epileptic seizures,and its antiepileptic effect may be realized through antioxidant effect.
关 键 词:戊四氮 癫痫 氧化应激 表没食子儿茶素没食子酸脂 神经保护作用
分 类 号:R741.2[医药卫生—神经病学与精神病学]
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