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[目的]探讨普罗布考对戊四氮所致癫痫大鼠的抗氧化作用及对海马神经元的保护作用.[方法]将SD雄性大鼠随机分为正常对照组、模型对照组及普罗布考组.采用Dihel点燃癫痫模型制作方法,实验持续14 d.观察模型对照组及普罗布考组大鼠癫痫发作潜伏期及发作持续时间,并测定各组大鼠海马组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量.采用HE染色法观察癫痫发作大鼠海马神经元形态学改变.[结果]普罗布考组大鼠发作潜伏期较模型对照组明显延长(P<0.01),发作时间显著缩短(P<0.05).普罗布考组大鼠海马神经元SOD活性与模型对照组相比较显著升高(P<0.01),与正常对照组比较明显降低(P<0.05).普罗布考组MDA含量与模型对照组比较显著降低(P<0.01),与正常对照组比较差异无统计学意义(P>0.05).HE染色结果见,普罗布考组坏死神经元与模型对照组比较显著减少(P<0.01).[结论]普罗布考可通过抗氧化机制来发挥抗癫痫作用,并对海马神经元起保护作用.
[Objective] To explore the antioxidative effect of probucol on pentylenetetrazole-induced epileptic rats and its protective effect on hippocampal neurons. [Methods] SD male rats were randomly divided into normal control group, model control group and probucol Test group.The method of making Dihel ignition epilepsy model was used and the experiment lasted for 14 days.The latency and duration of seizure in model control group and probucol group were observed.The superoxide dismutase ) Activity and the content of malondialdehyde (MDA) .Hematoxylin and eosin (HE) staining was used to observe the morphological changes of hippocampal neurons in seizure rats. [Results] The latency of rats in probucol group was significantly longer than that in model control group (P <0.01) (P <0.05) .The SOD activity of hippocampal neurons in probucol group was significantly higher than that in the model control group (P <0.01), and significantly lower than that in the normal control group (P <0.05) Compared with the normal control group, the content of MDA in the test group was significantly lower than that in the model control group (P <0.01), but there was no significant difference between the control group and the probucol group (P> 0.05) (P <0.01). [Conclusion] Probu Antiepileptic action may be through its antioxidant effects, and Neuroprotective Effect yuan.