| ObjectiveThe aim of this study was to investigate whether probucol has a preventive effect against epilepsy and post epileptic oxidative stress.Methed1. Experimental animals and grouping:The adult male SD rat (n=30) were divided into three groups:PTZ induced epilepsy group (n=10); probucol pre-disposal treatment group(n=10);control group(n=10).2.Make seizure kindling model:Basic on the Dihel's seizure kindling process,PTZ 50mg/kg i.p. to PTZ group and probucol group for seizure kindling model. The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration.3.make pre-disposal treatment:probucol group rats were treated with probucol 500mg/kg i.g for 14 days.4.Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), superoxide dismutase (SOD) were carried out in the hippocampal neurons. Observe the hippocampal neurons'damage by hematoxylin and eosin technique.Results1.All animals in PTZ group and probucol group were induces to seizure kindling.The grade of onset was determined by Racine's standatd after kindle. The latent period are longer in the probucol group than in PTZ induced epilepsy group (P < 0.01),and seizure period of probucol group was shorter than PTZ group.2.Biochemical analyses of hippocampal neurons, revealed a significant lower in the SOD levels in the seizure kindling models according to control group,PTZ group was much lower(p<0.05).MDA level in PTZ was higher than that in control group(p<0.01),and there was no significant change in probucol group.3. The results of HE stain:neurons of hippocampus in the control group were normal microscopically with HE stain.In the PTZ group, neuronal cell is more injuryed than probucol group.ConclusionThe present study demonstrated that probucol treatment both may increase latent interval and reduce seizure period,and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures.
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