Attenuation of axonal injury and oxidative stress by edaravone protects against cognitive impairments after traumatic brain injury

摘要: Abstract Traumatic axonal injury (TAI), a feature of traumatic brain (TBI), progressively evolves over hours through impaired transport and is thought to be major contributor cognitive dysfunction. In spite various studies suggesting that pharmacologic or physiologic interventions might reduce TAI, clinical neuroprotective treatments are still unavailable. Edaravone, free radical scavenger, has been shown exert effects in animal models several disorders. this study, evaluate whether edaravone suppresses TAI following TBI, mice were subjected weight drop had either (3.0 mg/kg) saline administered intravenously immediately after impact. Axonal oxidative stress assessed using immunohistochemistry with antibodies against amyloid precursor protein, marker transport, 8-hydroxy-2′-deoxyguanosine, DNA damage. Edaravone significantly suppressed the cortex, corpus callosum, hippocampus 24 h injury. The observed receiving 1.0, 3.0, 10 mg/kg impact, but not 0.3 mg/kg edaravone. With treatment 1 h was also therapeutic effect persisted up 6 h Furthermore, behavioral tests performed 9 days showed memory deficits saline-treated traumatized mice, which evident edaravone-treated group. These results suggest protects TBI protection mediated by suppression stress.