Abstract
Status epilepticus (SE) can cause severe neuronal loss and oxidative damage. Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) can be neuroprotective by inducing the antioxidant system, so we evaluated the role of PGC-1α in SE. The expression of PGC-1α and one of its target genes, uncoupling protein 2 (UCP2), was upregulated after SE, which may represent an endogenous neuroprotective mechanism. Furthermore, pretreatment with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor significantly attenuated both AMPK and PGC-1α activation, followed by downregulation of UCP2 and enhanced oxidative stress and hippocampal neuronal damage. AMPK/PGC-1α may be neuroprotective in SE-induced brain damage, at least in part via UCP2.
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