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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。
Objective: To study the antiepileptic effect and its mechanism. Methods: Intraperitoneal injection of PTZ was used to observe the epileptic seizure level. After that, each group was given valproic acid sodium (VPA) and different doses of APFmK for 7 days, and PTZ was injected again 4 hours after the last intragastric administration. At the episode level, the hippocampus was isolated and the changes of superoxide dismutase (SOD) and malondialdehyde (MDA) in the hippocampus were detected. RESULTS: AFBmK significantly reduced the incidence of attacks, increased SOD activity, and decreased MDA content. Conclusion: AFBmK can treat PTZ-induced mouse epilepsy. One of its mechanisms is to increase the activity of SOD in the hippocampus of mice, or to directly scavenge free radicals, increase the antioxidation level of hippocampal cells and reduce the peroxidation.