摘要
[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 study the antioxidative and protective effects of the probucol on hippocampus neurons in rats with epilepsy induced by cardiazol.METHODSThe SD rats were randomly divided into the control,model and probucol groups,and the experiment was continued for 14 days by the Dihel's seizure kindling process to observe the latency period and persistent period of seizure disorder in the model and probucol groups and to determine the activity of superoxide dismutase(SOD) and content of malondialdehyde(MDA) in the hippocampal tissue in each group.The morphological changes of hippocampal neurons of seizure disorder were observed by HE staining.RESULTS The latent period of epilepsy was longer in the probucol group than in model group(P0.01),and the period of seizure disorder was shorter than model group(P0.05).The activity of SOD in the hippocampal tissue was higher in the probucol group than in model group(P0.01),and lower than in control group(P0.05).The content of MDA in the hippocampal tissue was lower in probucol group than in model group(P0.01),and there was no significant difference as compared with the control group(P0.05).The number of necrotic neuron was significantly decreased in the probucol group than in model group(P0.01).CONCLUSIONThe probucol play a role of anti-epilepsy by antioxidative effects in rats,and protect the hippocampus neurons in rats with epilepsy induced by cardiazol.
出处
《延边大学医学学报》
CAS
2011年第1期12-14,共3页
Journal of Medical Science Yanbian University
关键词
癫痫
普罗布考
自由基清除剂
神经元
海马
大鼠
epilepsy
probucol
free radical scavengers
neurons
hippocampus
rats