Résumé
Objective To investigate neuroprotective effect of AM-36 on secondary brain injury following traumatic brain injury(TBI)in rats.Methods A total of 38 male Sprague-Dawley rats were divided into an experimental group,a control group and a sham operation group,then sustained to moder- ate TBI.AM-36(0.1 ml/100 g)was administered intraperitoneally in the experimental group and isoton- ic saline solution was administered intraperitoneally in the control and the sham operation groups at 30 mi- nutes,24 and 48 hours after TBI,respectively.The brain water content was determined at 24 hours after TBI.Rats were sacrificed by decapitation at 24 hours or one week after TBI for observing histological changes in peripheral cortex,thalamus and hippocampus by means of Hematoxylin and Eosin staining and Fluoro-Jade(F-J)staining.Results The brain water content of bilateral hemispheres 24 hours after TBI in the experimental group was significantly decreased,compared to that of the control group.Histo- logical examination revealed less degenerating neurons(F-J positive neurons)in the cortex,thalamus, CAI and CA3 of the hippocampus in AM-36 treated rats 24 hours and one week after injury(P＜0.05). Conclusion Systemic administration of AM-36 at the early stage after TBI can decrease brain water content and exert neuroprotective effect on TBI.F-J staining can be used for histopathologic quantitation of neuronal damage,for it can accurately exhibit pathologic changes following TBI induced by fluid per- cussion.