Abstract
The pathophysiology of neurological diseases related to potassium-channel dysfunction such as epilepsy is increasingly linked to immune system modulation. However, there are limited reports of which interleukin-4 (IL-4) can act on the neuroinflammatory response after seizure. Hence, we evaluated the effect of IL-4 in murine model of neuroexcitotoxcity using kaliotoxin (KTx), a potassium-channel blocker. Results showed that IL-4 treatment can significantly reduce the neuronal death induced by KTx. Probably by decreasing mitochondria swelling, reversing oxidative damage and enhancing Bcl-2 expression. Furthermore, IL-4 treatment significantly reduced TNF-α expression and enhanced GFAP and IL-10 expressions in the brain. IL-4 can be neuroprotective in epileptogenesis.
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