Change Of SOD, MDA And Mitochondrial Ultrastructure In The Hippocampal Of Epileptic Rats Induced By Lithium Chloride-Pilocarpine And The Effects Of Butyphthalide

PARTⅠTHE CHANGE OF SOD,MDA IN THE HIPPOCAMPUS OF EPILEPTIC RATS INDUCED BY LITHIUM CHLORIDE-PILOCARPINE AND THE EFFECTS OF BUTYPHTHALIDEObjective To investigate the alteration of behavior,the change of superoxide dismutase(SOD) and malondialdehyde(MDA) in the hippocampus of epileptic rats induced by lithium chloride-pilocarpine,and the protective effects of butyphthalide.Methods 30 adult male Wistar rats were randomly divided into intervention group(NBP,n=12),epilepsy group(SE,n=12)and control group(n=6),and the intervention group and epilepsy group were divided into 3h and 24h two point(each time point 6 rats).To establish the lithium chloride-pilocarpine temporal epilepsy model,the intervention group was given 80mg/Kg butyphthalide via i.p injection and the epilepsy group was given 80mg/Kg 0.9%NaCl the same way.Rats were killed 3 or 24hours at the end of lesion,and the hippocampus was taken out and levels of superoxide dismutase(SOD) and malondialdehyde(MDA) were determined. Results The average time of epilepsy group rats which developed seizures at stage 4 was 45.2±13min,The average time of NBP group rats which developed seizures at stage 4 was 75.8±15.6min,one of the rat didn't develop seizure. Compared with the NC group,the SOD activation obviously decreased at 3 hours (112.52±10.16) U/mgprot(p＜0.01) after SE in the epilepsy group,slightly increased at 24 hours(120.43±11.33) U/mgprot,but was still significantly different with the NC group(p＜0.05).MDA secretion increased over time,and was significantly different with the NC group at 3 hours(4.08±0.69nmol/ mgprot,p＜0.05)and at 24hours(5.24±1.55)nmol/mgprot,p＜0.01).The difference of the production of SOD(128.20±8.78)U/mgprot at 3 hour,(133.25±13.77U/mgprot at 24 hour) and MDA(3.50±0.12nmol/mgprot at 3 hour,3.94±0.89nmol/mgprot at 24 hour) between the NBP group and the NC group was not significant(P＞0.05).Conclusions Epileptic seizure could lead to the neuron injury by promoting hippocampus to secret more oxyradical,and inhibiting the ability of Scavenger. Butyphthalide can postpone the epileptic seizure,and protect the neuron by increasing the activation of SOD and decreasing the production of MDA.PARTⅡALTERATION OF MITOCHONDRIAL ULTRASTRUCTURE IN THE HIPPOCAMPUS OF EPILEPTIC RATS INDUCED BY LITHIUM CHLORIDE -PILOCARPINE AND THE EFFECTS OF BUTYPHTHALIDEObjective To investigate the alteration of mitochondrial ultrastructure in the hippocampus of epileptic rats induced by lithium chloride-pilocarpine,so to study the relation between mitochondria and epilepsy,to discuss the protective effect of butyphthalide. Methods 330 adult male Wistar rats were randomly divided into intervention group(NBP,n=12),epilepsy group(SE,n=12)and control group(n=6),and the intervention group and epilepsy group were divided into 3h and 24h two point(each time point 6 rats).To establish the lithium chloride- pilocarpine temporal epilepsy model,the intervention group was given 80mg/Kg butyphthalide via i.p injection and the epilepsy group was given 80mg/Kg 0.9%NaCl the same way.Rats were killed 3 or 24hours at the end of lesion,and part of the hippocampus was taken to be observed by light microscope and electron microscope.Results(1)HE staining:3h after SE,the structure of CA3 and gyrus dentatus between intervention group and control group were smiliar,epilepsy group occurred damaged such as celler swelling and hyperplasy;24h after SE,the structure of epilepsy group occurred more severe damaged such as celler disruption,neuron decreasing obviously,even cellular necrosis.The damage of intervention group was mild.(2) Electron microscope:in the epilepsy group,bioblasts were deformed,crista mitochondriales disappeared,there were cavitation and membranous body in the kytoplasm.In the intervention group,cellular construction was roughly normal,but the nucleoli collected aside,the construction of the chondriosome was still integrated. There were lessmembranous body,but the membrane broke and cristae mitochondriale depletion still appeared in some of the neurons.Conclusions The results demonstrate that mitochondrial ultrastructural damage in the hippocampus are associated with experimental temporal lobe epilepsy, indicating mitochondria were more vulnerable to epilepsy.Thus,butyphthalide can decrease the damage of the hippocampus neurons caused by temporal epilepsy.The mechanism is related to the protection effect of butyphthalide to the chondrosome.