The Change Of P38 And GAP-43 In Hippocampus Of Rats With Post-traumatic Epilepsy And The Intervention Effect Of Topiramate

ObjetiveEstablish an animal model of post-traumatic epilepsy by FeCl3 solution injection into the sensorimotor cortex of rats. Observe the characteristics of seizures. Detected the morphological changes of neuron in cortex and hippocampus of rats and the changes of P38 and GAP-43 expression in hippocampus, and observed the intervention effect of topiramate.Materials and methods108 adult male clean SD rats were randomly divided into 4 groups, normal control group, physiological saline control group, model control group, and TPM prevention group. The characteristics of seizures were observed everyday. Rats were sacrificed at different times, and the cortex and hippocampus of rats were stained with HE staining and nissl staining and the expression levels of P38 and GAP-43 in hippocampus were detected by immuneohistochemical method. Results1 Behavioral CharacteristicsThe average times of serious seizure of the TPM prevention group rats were lower than that of model control group, (P<0.05). The incubation period of 4 grades seizure of the TPM prevention group rats was longer compared with model control group(P<0.05).2 HE staining and Nissl stainingThe neuron number was normal in cortex and hippocampus of normal control group. The changes of neuron number of physiological saline control group were indistinct. The number of neuron in cortex and hippocampus were decreased of model control group, and the neuron number of TPM prevent group were higher compared with model control group.3 ImmunohistochemistryTo compared with normal control group, the expression of P38 and GAP-43 in hippocampus was increased of model control group(P<0.05), and the expression of P38 and GAP-43 in hippocampus of TPM prevent group rats was lower than that of the model control group rats(P<0.05).Conclusions1 The high expression of P38 and GAP-43 may play an important role in post-traumatic epilepsy.2 Topiramate may inhibit the forming of post-traumatic epilepsy by inhibiting the neuron necrosis and the high expression of P38 and GAP-43.