Abstract
Previous studies have indicated that hepcidin, which can regulate iron efflux by binding to ferroportin-1 (FPN1) and inducing its internalization and degradation, acts as the critical factor in the regulation of iron metabolism. However, it is unknown whether hepcidin is involved in acute renal ischemia/reperfusion injury (IRI). In this study, an IRI rat model was established via right renal excision and blood interruption for 45 min in the left kidney, and iron metabolism indexes were examined to investigate the change in iron metabolism and to analyze the role of hepcidin during IRI. From 1 to 24 h after renal reperfusion, serum creatinine and blood urea nitrogen were found to be time-dependently increased with different degrees of kidney injury. Regular variations in iron metabolism indexes in the blood and kidneys were observed in renal IRI. Renal iron content, serum iron and serum ferritin increased early after reperfusion and then declined. Hepcidin expression in the liver significantly increased early after reperfusion, and its serum concentration increased beginning at 8 h after reperfusion. The splenic iron content decreased significantly in the early stage after reperfusion and then increased time-dependently with increasing reperfusion time, and the hepatic iron content showed a decrease in the early stage after reperfusion. The early decrease of the splenic iron content and hepatic iron content might indicate their contribution to the increase in serum iron in renal IRI. In addition, the duodenal iron content showed time-dependently decreased since 12 h after reperfusion in the IRI groups compared to the control group. Along with the spleen, the duodenum might contribute to the decrease in serum iron in the later stage after reperfusion. The changes in iron metabolism indexes observed in our study demonstrate an iron metabolism disorder in renal IRI, and hepcidin might be involved in maintaining iron homeostasis in renal IRI. These findings might suggest a self-protection mechanism regulating iron homeostasis in IRI and provide a new perspective on iron metabolism in attenuating renal IRI.
Highlights
Ischemia/reperfusion injury (IRI) is a common pathogenesis of acute kidney injury (AKI) because the kidneys are highly perfused organs and are very sensitive to ischemia
The serum creatinine (SCr) and blood urea nitrogen (BUN) levels were significantly elevated in the IRI groups compared with levels in the control group, and both SCr and BUN
Based on the RT-polymerase chain reactions (PCRs) analysis, we found that hepcidin mRNA levels in the liver were significantly increased in the IRI groups compared with levels in the control group
Summary
Ischemia/reperfusion injury (IRI) is a common pathogenesis of acute kidney injury (AKI) because the kidneys are highly perfused organs and are very sensitive to ischemia. Iron metabolism in renal ischemia/reperfusion injury procedures and factors can result in renal IRI, such as renal vascular surgery, kidney transplant, cardiac arrest, hypotension and shock [1] IRI is a pathological phenomenon in which renal tissue and cell damage are caused by ischemic aggravation after blood reperfusion, which is a key factor leading to renal failure and a poor prognosis. Studies have shown that iron itself and iron-related oxidative stress may play important roles in kidney injury under pathologic conditions [3]. Iron can catalyze the generation of hydroxyl free radicals and lipid peroxidation, leading to oxidative stress and tissue damage [5]. These findings suggest that iron metabolism disorder may occur during IRI
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