Objective: 

Hepcidin is a small peptide hormone having a central role for regulating iron metabolism. Hepcidin decreases release of iron from macrophages and enterocytes and blocks the iron transport from enterocyte to plasma by internalizing of ferroportin, a channel protein for iron export. Myocardial ischemia causes increase in the ferritin stores in the cardiac muscle in a dose dependent manner. The iron stores in cardiac myocytes cause oxidant stress in cardiomyocytes. In addition, fenton reaction causes hydrogen peroxide production and it causes DNA damage by changing myocardial function. Hepcidin is also secreted from cardiac myocyte and its release is regulated by hypoxia and inflammation. The scope of this investigation is to test the effect of hepcidin on cardiac ischemia reperfusion for oxidative stress.

Methods: 

Wistar-Albino rat hearts (n=12) were loaded on Langendorff system perfusing with Krebs-Henseleit solution. Hepcidin was applied at the onset of no flow ischemia (n=6). In control group (n=6) no substance was applied. MDA, GSH and NOx determinations were made in heart muscle by biochemical methods.

Results: 

MDA and NOx levels were decreased (p<0.05), but GSH levels did not change significantly in hepcidin applied group (p>0.05).

Conclusions: 

Hepcidin protected heart muscle from oxidant factors stress by inhibiting NOx and lipid peroxidation and by preserving antioxidant systems.