To strengthen a pivotal role of the PPARγ/UCP2 signaling pathway in oxidative stress damage in the hippocampus following experimental status epilepticus, we observed that bilateral microinjection of rosiglitazone into the hippocampal CA3 region, at a dose (6 nmol) that enhanced UCP2 expression, also decreased the levels of O2·- ((Figure 6A) or oxidized protein (Figure 6B) in the CA3 subfield 24 h after KA-induced experimental status epilepticus. This evidence concerns the gene PPARG and status epilepticus.