| Objective: Trauma brain injury often associated with brain edema occurred.Recent evidences suggest that AQP-4 contribute to acute edema and lesion formation following brain ischemic lesion and TBI. Many experimental and clinical studies have reported that hyperbaric oxygen therapy (HBOT) may be beneficial in craniocerebral injury. The mechanisms of the beneficial effects of HBOT are not clearly understood.The purpose of this study was to evaluate the effects of HBOT on the expression of AQP-4 in the rat model of TBI.Methods: Male Sprague–Dawley rats were traumatized by the Feeney's brain injury model. The rats were randomly divided into three groups(n=32 for each group): sham-operated, TBI with subsequent HBOT (2ATA),and not treated after TBI。The animals were killed at 12h,1day,3days and 5 days. Immunohistochemical staining for AQP-4 and behavior outcomes was also performed and the results were quantitatively evaluated by image analysis.Results: The protein expression of AQP-4 was less in normal brain tissue.The positive expression was mainly distributed at the endyma of cerebral ventricle and aqueduct, piamater and foot process of astrocyte around microvessel.From 12 hours after operation, there was more protein expression of AQP-4 expressed by foot process of astrocyte cell in contusion marginal region in TBI group, reached summit 24h after operation, degraded 3 days.The expression of AQP-4 in HBOT group decreased significantly compared with TBI group (P<0.05). In the animals treated by HBOT, behavior outcomes were significantly improved comparison with that in the nontreated animals.Conclusions: The decline of AQP-4 expression after HBOT may contribute to protection of brain tissue in the perilesional area. |
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