RESUMEN
Objective To explore the neuroprotective effects ofβ-aescinate on brain edema in rats of traumatic brain injury (TBI). Methods A total of 78 male SD (Sprague Dawley) rats were randomly divided into three groups: sham-operation group (Sham), traumatic brain injury group (TBI) andβ-aescinate group, with 26 rats in each group. Rats of Sham group were anesthetized and surgically prepared only, but were not induced by cortical contusion. Electronic brain cortical damage impactor (eCCI) was used for establishing TBI model in TBI group and β-aescinate group after opening the bone window. TBI group was only established TBI model, but no intervention. After establishment of TBI model in β-aescinate group, β-aescinate (5 mg/kg body weight) was intraperitoneally injected, once every 24 hours. The modified neurological severity scores (mNSS) was used for evaluating changes of neurological function. After 48 hours, SD rats were sacrificed for hematoxylin and eosin (H&E) staining (n=6). Additionally, water content of the brain tissue was evaluated using the wet-to-dry weight ratio (n=10). Evans blue assay was performed to investigate the blood-brain barrier (BBB) permeability (n=4). The expression of aquaporin 4 (AQP4) was measured by Western blot assay (n=6). Results Compared with the Sham group, neurologic deficit, increased brain water content and the expression of AQP4 were found in TBI group (all P<0.05). Moreover, BBB permeability was destroyed. However, β-aescinate can improve the neurological function, reduce the brain water content and significantly decrease the expression of AQP4 in TBI rats. The BBB permeability was significantly improved in treatment group (all P<0.05). Conclusion These findings suggest that β-aescinate can reduce cerebral edema and improve neurological outcome in SD rats after TBI. This neuroprotection may be related with the down-regulation of AQP4 protein.