Myelin sheath, either in white matter or in other regions of brain, is vulnerable to
ischemia. The specific events involved in the progression of
ischemia in white matter have not yet been elucidated. The aim of this study was to determine histopathological alterations in cerebral white matter and levels of
myelin basic protein (MBP) in
ischemia-injured brain tissue during the acute and subacute phases of central nervous injury following whole-
brain ischemia. The whole
cerebral ischemia model (four-vessel occlusion (4-VO)) was established in adult Sprague-Dawley rats and MBP gene expression and
protein levels in the brain tissue were measured using reverse transcription-polymerase chain reaction and
enzyme-linked
immunosorbent assay (ELISA) at 2 days, 4 days, 7 days, 14 days, and 28 days following
ischemia.
Demyelination was determined by
Luxol fast blue myelin staining, routine histopathological staining, and electron microscopy in injured brain tissue. Results showed that
edema, vascular dilation, focal
necrosis,
demyelination, adjacent reactive
gliosis and
inflammation occurred 7 days after
ischemia in HE staining and recovered to control levels at 28 days. The absence of
Luxol fast blue staining and vacuolation was clearly visible at 7 days, 14 days, and 28 days. Semiquantitative analysis showed that the transparency of myelin had decreased significantly by 7 days, 14 days, and 28 days.
Demyelination and ultrastructual changes were detected 7 days after
ischemia. The relative levels of MBP
mRNA decreased 2 days after
ischemia and this trend continued throughout the remaining four points in time. The MBP levels measured using ELISA also decreased significantly at 2 days and 4 days, but they recovered by 7 days and returned to control levels by 14 days. These results suggest that the impact of
ischemia on cerebral white matter is time-sensitive and that different effects may follow different courses over time.