| Objective:Peroxisome proliferators activated receptor gamma (PPARs) is a ligand-activated transcriptional fator. It plays a neuroprotective role in cerebral ischemic disease, Parkinson's disease, Alzheimer's disease, and other nervous system diseases by anti-inflammatory, anti-oxidation, anti-apoptotic and other mechanisms when it is activated. In the present investigation we evaluated the effects of PPAR agonist rosiglitazone onto the hippocampus of status epilepticus rats.By contrasting the expression of Bcl-2,Bax protein and the number of TUNEL-positive cells in hippocampus after pilocarpine-induced status epilepticus,the protective effect of rosiglitazone on rats status epilepticus can be evaluated and the mechanism of this medicine can be studied.Methods:Fifty-four healthy adult male Wistar rats were randomly divided into three groups:the model control group(n=24), the model treatment group (n=24)(each group is further divided into four sub-groups depending on the time, each sub-groups is six) and normal control group (n=6).Each group is treated with the method of gavage. The control group and the model group are given equal volume saline. The model treatment group rats are given rosiglitazone solution (4mg/kg/d). Five days after gavaged, Lithium Chloride (127 mg/kg, i.p.) was injected 18 h prior to the administration of freshly prepared pilocarpine(30 mg/kg, i.p.).The control group rats received all treatment with saline instead of Lithium Chloride or pilocarpine. The model treatment group rats survived status epilepticus were gavaged with rosiglitazone(4mg/kg) every 24 hours, while the rats of model control group and normal control group were given same volume of saline. The model control group and the model treatment group rats were sacrificed, respectively, at 12 h,24 h,72 h,7 d after SE. The control group rats were killed together with rats that were sacrificed 12 h after SE. The hippocampus of all study object were given TUNEL staining to measure apoptotic cell and given immunohistochemistry analysis to test Bcl-2, Bax,at the same time the ratio of Bcl-2/Bax was calculated. SPSS 13.0 version was used for statistical analysis and P<0.05 was regared as statistical significance.Result:TUNEL, Bcl-2 and Bax positive cells in hippocampus of model group compared with that of normal saline control group were increased significantly(P<0.05). Bax and TUNEL positive cells in the rosiglitazone group compared with that in the model group were reduced significantly(P<0.05). The TUNEL positive cells began to express in hippocampus of the model group and the rosiglitazone group at 12h after SE, then they increased and reached peak level at 48h, after this, the level of TUNEL positive cells began to decrease gradually till to 7d. The Bax positive cells began to express in hippocampus of the model group and the rosiglitazone group at 12h after SE, then they increased and reached peak level at 24h, after this, the level of Bax positive cells began to decrease gradually till to 7d. Bcl-2 positive cells and Bcl-2/Bax ratio in the rosiglitazone group compared with that in the model group were increased significantly(P<0.05).The Bcl-2 positive cells began to express significantly in hippocampus of model group at 12h after SE, then the expression of them began to decrease gradually to the level of control group in 7d. The Bcl-2 positive cells began to express in hippocampus of rosiglitazone group at 12h after SE, then they increased and reached peak level at 24h, after this, the level of Bcl-2 positive cells decreased.The peak of the Bcl-2/Bax ratio in the model group and the rosiglitazone group were all at 12h after SE, and then declined.Conclusion:(1) The present study shows that PPAR agonist, rosiglitazone, has protective role against post-status epilepticus neuroton injury in rat.(2)The protective role of rosiglitazone against post-status epilepticus neuroton injury in rat is related with the mechanism effect of anti-apoptosis.
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