目的:研究SD大鼠肾缺血再灌注损伤(IRI)后铁代谢的变化特点,探讨IRI后铁调素和铁代谢的变化及意义。方法:雄性SD大鼠48只,随机分为对照组(n=6)和IRI模型组,模型组分别在IRI后1h、4h、8h、12h、16h、20h、24h 7个时间点(n=6/组),检测大鼠血生化及铁代谢指标,以及肝组织铁调素mRNA和肾组织膜转铁蛋白1(FPN1)mRNA和蛋白的表达水平。结果:与对照组相比,IRI组肾组织铁含量、血清铁、铁蛋白在再灌注早期升高(P<0.05),并随再灌注时间的延长逐渐下降。IRI组肝组织铁调素mRNA表达水平在再灌注早期明显升高,再灌注4h达峰值后开始下降,而血清铁调素于再灌注8h后升高,并于再灌注16h达峰值后开始下降,两者在再灌注24h后仍高于对照组(P<0.05)。IRI组肾组织FPN1 mRNA和FPN1蛋白的表达水平随再灌注时间的延长逐渐下降,两者表达水平明显低于对照组(P<0.05)。结论:大鼠肾脏IRI过程中伴有铁代谢的紊乱,铁调素和肾脏FPN1可能参与了IRI过程中铁稳态的调控。 OBJECTIVE: To study the changes of iron metabolism after renal ischemia-reperfusion injury (IRI) in SD rats and to explore the changes and significance of hepcidin and iron metabolism after IRI. Methods: Forty-eight male Sprague-Dawley rats were randomly divided into control group (n = 6) and IRI model group. The rats in model group were injected intraperitoneally with different time points after IRI for 1 hour, 4 hours, 8 hours, 12 hours, 16 hours, 20 hours, 6 / group). The indexes of blood biochemical and iron metabolism, as well as hepatic hepcidin mRNA and renal tissue membrane transferrin 1 (FPN1) mRNA and protein expression were detected. Results: Compared with the control group, the iron content in renal tissue, serum iron and ferritin in IRI group increased at early reperfusion (P <0.05), and decreased gradually with the reperfusion time prolonged. The expression of hepcidin mRNA in liver tissue of IRI group increased significantly at the early stage of reperfusion, reached the peak at 4h after reperfusion, but decreased at 8h after reperfusion, and began to decrease after 16h of reperfusion , Both of which were still higher than those of the control group 24h after reperfusion (P <0.05). The expression of FPN1 mRNA and FPN1 protein in renal tissue of IRI group decreased gradually with the prolongation of reperfusion time, the expression levels of both were significantly lower than those of control group (P <0.05). CONCLUSION: Iron metabolism is associated with IRI in rat kidney, and hepcidin and renal FPN1 may be involved in the regulation of iron homeostasis during IRI.