It is intriguing that results from the present study also showed that pretreatment with rosiglitazone increased mitochondrial UCP2 expression, reduced the extent of protein oxidation, O2·- overproduction and dysfunction of mitochondrial respiratory enzyme complex I, hindered the translocation of Bax or cytochrome c between cytosol and mitochondria and reduced neuronal damage in the hippocampal CA3 subfield elicited by experimental status epilepticus. This evidence concerns the gene BAX and status epilepticus.