We demonstrated that activation of PPARγ upregulated mitochondrial UCP2 expression, which decreased overproduction of ROS, improved mitochondrial complex I dysfunction, inhibited mitochondrial translocation of Bax and prevented cytosolic release of cytochrome c by stabilizing the mitochondrial transmembrane potential, leading to amelioration of apoptotic neuronal cell death in the hippocampus following status epilepticus. This evidence concerns the gene BAX and status epilepticus.