Abstract:

Abstract： ObjectiveTo study the effects of Edaravone on cognitive  function and its potential mechanism after traumatic brain injury. MethodsMale SpragueDawley rats were randomly divided into the control group（n=40），　the traumatic group（n=68），　and the Edaravone treatment group（68）. TBI rat models were established based on description of the Marmarou′s diffused brain injuries. At 1，6，24，48，72?h after injuries， the histopathological changes of mitochondria were observed with an electron microscope. Expressions of pERK1/2 and Cytc were determined by immunohistochemistry and WesternBlot. Learning and memory functions (Morris water maze) were determined daily 3?d after injuries for 7?d. ResultsAfter TBI， some mitochondria displayed swelling, spinal fracture, or even disappeared. Expression of pERK1/2 increased with the development of TBI and peaked at 24 h, then gradually decreased and expression of Cytc increased and peaked at 48?h. The searching safety island period山of rats in the traumatic group(230.9±20.9) was significantly longer than that of rats in the control group(50.7±4.9). While the histopathological damages of mitochondria and expressions of pERK1/2 and Cytc were significant decreased in the Edaravone treatment group, and the searching safety island period (130.0±30.8) was markedly restored(P＜0.05). ConclusionEdaravone has good therapeutic effect on traumatic brain injury and the molecular mechanism is related to attenuating ERK1/2 activation and Cytc release following the trauma.

Key words:  Brain injuries； Mitogenactivated protein kinases； Cytochrome  c； Edaravone