BACKGROUND: Iron is an important micronutrient for neuronal function and survival.It plays an essential role in synthesis of the myelin sheath and neurotransmission.On the contrary, iron also catalyses the production of free radicals and hence, causes oxidative stress.Therefore, maintenance of iron homeostasis is very crucial and it involves a number of proteins in iron metabolism and transport that maintain the balance.Iron distribution and expression of iron transmembrane protein in cerebral ischemia are unknown.In this study, we focus on the changes of iron transmembrane protein expression,such as Transferrin Receptor (TFR), Ferroportin (Fpn), Feline leukemia virus subgroup C receptor (FLVCR) and Breast cancer resistance protein (BCRP), in the rat hippocampus following focal cerebral ischemia.METHODS: Rats were randomly divided into 2, 6, 12, 24 and 72 h groups following middle cerebral artery occlusion (MCAO) and the mRNA and protein level of iron transmembrane proteins were detected by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR) at the above time points respectively.RESULTS: The expression of TFR was significantly increased in the hippocampus at 12h after surgery and maintained in a high level at 24h and 72h (P<0.05), whereas BCRP was reduced at 12h after surgery and maintained at low level at 24h and 72h.The expression level of FLVCR was significantly decreased at 72h, while the expression of Fpn was increased, which is reached a peak at 12h after surgery.CONCLUSIONS: Our findings strongly suggest that dysregulation of intracellular iron balance is possibly a new mechanism underlying cerebral ischemia and that targeting iron homeostasis may serve as a Potential therapeutic approach to combat cerebral ischemia.