Hypoxic-ischemic white matter injury (WMI) pathogenesis in preterm infants is not well established, and
iron-related
proteins in the brain may play an important role in imbalanced
iron metabolism. We aimed to investigate the
iron-related
protein changes in neonatal rats after
hypoxia-
ischemia (HI), clarify the role of
iron-related
proteins in hypoxic-ischemic WMI, and potentially provide a new target for the clinical treatment of hypoxic-ischemic WMI in preterm infants. We adopted a WMI animal model of bilateral common carotid artery
electrocoagulation combined with
hypoxia in neonatal 3-day-old Sprague-Dawley rats. We observed basic
myelin protein (MBP) and
iron-related
protein expression in the brain (
ferritin,
transferrin receptor [TfR], and membrane
iron transporter 1 [FPN1]) via Western blot and double immunofluorescence staining. The expression of MBP in the WMI group was significantly downregulated on postoperative days (PODs) 14, 28, and 56.
Ferritin levels were significantly increased on PODs 3, 7, 14, and 28 and were most significant on POD 28, returning to the
sham group level on POD 56. FPN1 levels were significantly increased on PODs 7, 28, and 56 and were still higher than those in the
sham group on POD 56. TfR expression was significantly upregulated on PODs 1, 7, and 28 and returned to the
sham group level on POD 56. Immunofluorescence staining showed that
ferritin, TfR, and FPN1 were expressed in neurons, blood vessels, and oligodendrocytes in the cortex and corpus callosum on POD 28. Compared with the
sham group, the immune-positive markers of three
proteins in the WMI group were significantly increased. The expression of
iron-related
proteins in the brain (
ferritin, FPN1, and TfR) showed spatiotemporal dynamic changes and may play an important role in hypoxic-ischemic WMI.