Abstract
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.
Highlights
Spontaneous subarachnoid hemorrhage (SAH) is usually caused by a ruptured intracranial aneurysm
By Western blot, CD163 protein levels in ipsilateral cortex were upregulated after SAH, peaking at day 1(CD163/β-actin: 1.22 ± 0.31 vs. 0.09 ± 0.06 in sham, p < 0.01)
The main findings from our study are as listed below: (1) CD163 protein levels were elevated in rat brain following SAH; (2) CD163 protein was expressed by neurons, microglia/macrophages, and oligodendrocytes; (3) CD163positive cells were cleaved caspase-3-positive, indicating that CD163 positive cells could be apoptotic cells; and
Summary
Spontaneous subarachnoid hemorrhage (SAH) is usually caused by a ruptured intracranial aneurysm. It is a form of stroke with a high mortality rate and early brain injury after SAH is an important factor contributing to death and disability. Hemoglobin released from red blood cells induces cell death and brain injury in intracerebral hemorrhage (ICH) and SAH (Xi et al, 2006; Lee et al, 2010). Such damage may be limited by hemoglobin clearance and degradation. Western blot and immunohistochemistry was used to assess CD163 expression following SAH
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