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- W821609122 abstract "Objective To study the effects of Edaravone on cognitive function and its potential mechanism after traumatic brain injury.Methods Male 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.Results After 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 periodof 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(P0.05).Conclusion Edaravone 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." @default.
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- W821609122 date "2009-01-01" @default.
- W821609122 modified "2023-09-27" @default.
- W821609122 title "Effect of Edaravone on cognition ERK1/2 activation and Cytc release after traumatic brain injury in rats" @default.
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