| Epilepsy is one kind of chronic clinical common syndrom, it's pathogenesis is very complicated. Forthcoming clinical observation and laboratory finding show that the children with epilepsy have immune disorders. Microglia cell as the macrophage of the central nervous system can activate to start a machine of endogenous immunologic response reaction quickly as soon as the damage occurs. Cell population, cell shape, transmutation of plasticity of cell surface molecule indicate that activation of microglia. OX42 is miceoglia peculiarity marker. Glucocorticoid as one kind of neuromodulator to regulate cranial nerve and endocrine. The study and research show that glucocorticoid and its acceptor is connected with epilepsy morbidity, so we can think glucocorticoid to have inhibitory and decreasing seizure of epilepsy. But the mechanism and the effect link are not still clear, in order to investigate the effect of glucocorticoid in the course of epilepsy and interpret the therapeutical effect of glucocorticoid ,we observe the expression of microglia within hippocampus of seizure rat induced by Kainic acid (KA).Objectives: In order to investigate the effect of dexamethsone on the seizure model, we observe the behavior, electroencephalogram and morphologic change of microglia in CA3 region of hippocampus of rats.Methods1 Animals and groups49 healthy male Sprague-Dawley rats are divided into three group according to digital table follow the random principle: 1)normal control group; 2) KA induced seizure group+normal saline control(KA+NS); 3) KA induced seizure group+dexame -thsone (KA+DEX),KA +NS group's rats peritoneal injection a dose of 0.5mg/kg.d saline in advance. KA+DEX group's rats received a dose of 0.5mg/kg.d DEX.2 Behavior observationAccording to Diehl stage of seizure observe and record the behavior of the rats, after injection KA into CA3 field of hippocampus.3 Electroencephalogram recordingFix position placing cortex electrode and hippocampus electrode, reference electrode go to the tip of the nose. Paper-speed was 30mm/s,sensitivity was 20uv/mm, record time lasting 30min.4 ImmunohistochenistryRats of KA+NS group and KA+DEX group were perfused at the time 3 hours ,24 hours, 7 days after inject KA, take the brain tissue between the midbrain and the bulbus gray. 15% and 30% cane sugar solution grad dehydration successively, the frozen section were cut with 40um in thickness and immunochemistry-strained with OX42 (1:300) according to standard procedures. After observation and photography, counted the OX42 positive cells within CA3 region of hippocampus.Results1 Change in behavior in ratsKA+NS group and KA+DEX group have eleptiform seizure after inject KA , no manifest difference between the two groups.2 EEG resultThe obvious epileptic electric discharge in KA+NS group, it included abnormal spikes, spike-wave complexes. The EEG records of KA+NS group contained epileptic electric discharge in a low degree; both the frequency and amplitude are lower than KA+NS group.3 Immunohistochemistry resultsTo compare with the normal control, the OX42 positive cell's number of the KA+NS group and the KA+DEX group increased obviously.3 hours group: OX42 positive cell showed actively ,the staining of them was condense, the number of them was increased, arrangement is confused, While there is no obviously difference between the KA+NS group and the KA+DEX group.48 hours and 7 days group : the expression of OX42 has significant difference between the KA+NS group and the KA+DEX group.ConclusionThe results indicated that small dosage dexamethasone administration before inducing seizures can suppress the activation of microglia to a certain extent. |
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