Despite advances in diagnosis and treatment of subarachnoid hemorrhage (SAH), combined morbidity and mortality rate in SAH patients accounted for greater than 50%. Many prognostic factors have been reported including delayed cerebral ischemia, cerebral vasospasm-induced infarction, and shunt-dependent hydrocephalus as potentially preventable or treatable causes. Recent experimental studies emphasize that early brain injury, a concept to explain acute pathophysiological events that occur in brain before onset of cerebral vasospasm within the first 72 h of SAH, may be more important than cerebral vasospasm, a classically important determinant of poor outcome, in post-SAH outcome. Galectin-3 is known for one of matricellular proteins and a mediator of inflammation in the central nervous system. Galectin-3 was also reported to contribute to poor outcomes in SAH patients, but the role of galectin-3 after SAH has not been determined. We produced experimental SAH mice, of which the top of the internal carotid artery was perforated by 4-0 monofilament, and evaluated effects of a galectin-3 inhibitor. We assessed neurological scores and brain water content at 24 h. The administration of a galectin-3 inhibitor significantly ameliorated brain edema and neuronal score in experimental SAH mice.
Keywords: Early brain injury; Galectin-3; Subarachnoid hemorrhage.