Abstract:

Ｏｂｊｅｃｔｉｖｅ：To investigate iron metabolism in rat after renal ischemiareperfusion injury (IRI), and probe into the change and significance of iron metabolism after renal IRI in rat.
Ｍｅｔｈｏｄｏｌｏｇｙ：A total of 48 SpragueDawley rats were randomly divided into IRI group (n=42) and control group (n=6)．The rats in IRI group were also divided into seven subgroups (n=6 each)：IRI 1h, IRI 4 h, IRI 8 h, IRI 12 h, IRI 16 h, IRI 20 h, and IRI 24 h. After the IRI model was established successfully, the blood biochemical and iron metabolism indexes, the expression level of hepcidin mRNA in the liver and ferroportin 1 (FPN1) mRNA and protein in the kidney were measured and analyzed.
Ｒｅｓｕｌｔｓ：Serum creatinine and blood urea nitrogen were timedependent increased in the IRI group than those in the control group (P<005). Compared with the control group, renal iron content, serum iron and serum ferritin in the IRI group were increased early after renal ischemia reperfusion  (P<005), and then declined. The expression level of hepcidin mRNA in the liver was significantly increased early after renal reperfusion, and the serum concentrations of hepcidin increased obviously since 8h after renal ischemia reperfusion in the IRI group  (P<005). The expression level of FPN1 mRNA and FPN1 protein in the kidney was declined obviously after renal ischemia reperfusion in the IRI group  (P<005). 
Ｃｏｎｃｌｕｓｉｏｎ：Iron metabolism disorder exists in rats during renal IRI, hepcidin in the liver and FPN1 in the kidney may participate in the regulation of iron homeostasis during renal IRI.