Hemoglobin contributes to brain cell damage and death following subarachnoid hemorrhage (SAH). While CD163, a hemoglobin scavenger receptor, can mediate the clearance of extracellular hemoglobin it has not been well-studied in SAH. In the current study, a filament perforation SAH model was performed in male rats. T2-weighted and T2*-weighted scans were carried out using a 7.0-Tesla MR scanner 24 h after perforation. T2 lesions and hydrocephalus were determined on T2-weighted images. A grading system based on MRI was used to assess SAH severity. The effects of SAH on CD163 were determined by immunohistochemistry staining and Western blots. SAH led to a marked increase in CD163 levels in cortex, white matter and periventricular regions from days 1 to 7. CD163 stained cells were co-localized with neurons, microglia/macrophages, oligodendrocytes and cleaved caspase-3-positive cells, but not astrocytes. Furthermore, CD163 protein levels were increased in rats with higher SAH grades, the presence of T2 lesions on MRI, or hydrocephalus. In conclusion, CD163 expression is markedly upregulated after SAH. It is associated with more severe hemorrhage, as well as MRI T2 lesion and hydrocephalus development.
Keywords: CD163; T2 lesion; hydrocephalus; magnetic resonance imaging; subarachnoid hemorrhage.