| Objective: To observe the iron content and the expression of Hepcidinin early period after subarachnoid hemorrhage (SAH) in rats, and toinvestigate whether disorder of brain iron metabolism mediated byHepcidin participated in the mechanism of apoptosis after SAH.Methods: Totally90adult male SD rats were randomly divided into2groups, the sham-operation group and SAH group. The SAH model wasestablished by single blood injection to prechiasmatic cistern.Immunohistochemical and Western Blotting were adopted to examined theexpression of Hepc at12,24,48,72h after SAH. Meanwhile, the iron contentwas detected by Atomic Absorption Spectrometer.Results: In Immunochemistry, Compared with the level of the shamgroup(0.19±0.05), Hepcidin expression in rats in SAH group began to riseat12h(0.30±0.06), the level was gradually increased over time until72h(0.56±0.07). The expression of Hepc in SAH group was significantlyhigher than that of the sham group (F=31.911, P<0.05). In western blot,Compared with the level of the sham group(0.238±0.047), Hepcidinexpression in rats in SAH group began to rise at12h(0.481±0.065), the level was gradually increased over time until72h(1.627±0.143). Theexpression of Hepc in SAH group was significantly higher than that of thesham group After SAH modeling,(F=147.314,P<0.05).Iron content inSAH group began to rise at12h after SAH(58.50±9.19), and wasgradually increased until72h(99.34±7.68), the contents in each time pointswere higher than that in sham group(43.51±4.59)(F=28.799,P﹤0.05).The expression of Hepcidin was correlated with the iron content in SAHgroup(r=0.914,P﹤0.01).Conclusion: Experimental SAH induces Hepcidin upregulation inearly stage after injury, the which may be associated with the increasedbrain iron content in early stage after experimental SAH. |