Abstract
Oxidative stress has been considered as one of pathogenesis of brain damage led by epilepsy. Reducing oxidative stress can ameliorate brain damage during seizures. However, expression levels of important antioxidative enzymes such as thioredoxin-1 (TRX1), thioredoxin-like 1 protein (TXNL1) and thioredoxin reductase 1 (TXNRD1) during seizures have not been investigated. In this study, we examined protein and mRNA expression levels of TRX1, TXNL1 and TXNRD1 in different brain regions in PTZ induced seizure model mice. We found that protein expression levels of TRX1, TXNL1 and TXNRD1 are simultaneously up-regulated by 2- or 3-fold in the cortex of both acute and chronic seizure model mice. But there is no unified expression pattern change of these enzymes in the hippocampus, cerebellum and diencephalon in the seizure model mice. Less extent up-regulation of mRNA expression of these enzymes were also observed in the cortex of seizure mice. These data suggest that antioxidative enzymes may provide a protective effect against oxidative stress in the cortex during seizures.
Highlights
Epileptic seizure is excessive and abnormal neuronal activity from a specific region of the brain, which may lead to convulsion, decreased level of consciousness, and other sensory or motor symptoms
Our results showed that proteins and mRNA expression levels of TRX1, thioredoxin-like 1 protein (TXNL1) and TXNR1 are up-regulated in the cortex in the PTZ kindled seizure mice
We present data showing protein and mRNA of important reductases are distinctly regulated in different brain regions in PTZ induced acute and chronic seizure model mice
Summary
Epileptic seizure is excessive and abnormal neuronal activity from a specific region of the brain, which may lead to convulsion, decreased level of consciousness, and other sensory or motor symptoms. Causes of epilepsy include all kinds of genetic ion channel mutations, altered cortical development and specific gene expression changes [1,2,3,4]. Frequent seizures may lead to neurodegeneration and generate oxidative stress by hyper-excitability. During abnormal excitable neuronal synaptic release process, activation of ionotropic glutamate receptor triggers elevated intracellular Ca2+ entry at cellular level in the nervous system.
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