Post-treatment of an NADPH oxidase inhibitor prevents seizure-induced neuronal death

Post-treatment of an NADPH oxidase inhibitor prevents seizure-induced neuronal death
Temporal lobe epilepsy Seizure NADPH oxidase Reactive oxygen species Blood brain barrier Neurodegeneration Microglia Neurotrophil infiltration
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Series/Report no.
BRAIN RESEARCH ; Vol1499 Startpage 163 Endpage 172
The present study sought to evaluate the neuroprotective effects of apocynin, an NADPH oxidase assembly inhibitor, on seizure-induced neuronal death. Apocynin, also known as acetovanillone, is a natural organic compound isolated from the root of Canadian hemp (Apocynum cannabium). It has been extensively studied to determine its disease-fighting capabilities and application in several brain insults, such as traumatic brain injury and stroke. Here we tested the hypothesis that post-treatment of apocynin may prevent seizure-induced neuronal death by suppression of NADPH oxidase-mediated superoxide production. Temporal lobe epilepsy (TLE) was induced by intraperitoneal injection of pilocarpine (25 mg/kg) in male rats. Apocynin (30 mg/kg, i.p.) was injected into the intraperitoneal space two hours after seizure onset. A second injection was performed 24 h after seizure. To test whether apocynin inhibits NADPH oxidase activation-induced reactive oxygen species (ROS) production, dihydroethidium (dHEt, 5 mg/kg, i.p.) was injected before onset of seizure and ROS production was detected five hours after seizure onset. Neuronal oxidative injury (4HNE), neuronal death (Fluoro Jade-B), blood brain barrier (BBB) disruption (IgG leak), neurotrophil infiltration (MPO) and microglia activation (CD11b) in the hippocampus was evaluated at three days after status epilepticus (SE). Pilocarpineinduced seizure increased p47 immunofluorescence in the plasma membrane of hippocampal neurons at 12 h post-insult and apocynin treatment prevented this increase.
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