Oxygen free radicals contribute to various kinds of tissue injury processes within the central nervous system. It has been suggested that inhibition of
free radical formation has the potential to attenuate secondary neural tissue damage involving
ischemia or
trauma, and
antioxidant therapy may offer a promising approach. In the present study, employing a
cortical contusion model in the rat,
contusion-induced neural damage, was evaluated by investigating
edema formation, behavioral activities and histological changes. The effects of the
superoxide radical scavenger,
OPC-14117, were also tested to determine how
free radicals may contribute to such neural damage. The results demonstrated that
cerebral contusion induces a progressive decrease in tissue specific gravity representing
edema formation, and behavioral deficits in the Morris water maze test and habituation of exploratory activity. Histological examinations revealed necrotic cavity formation in the cortex and selective neuronal death of the hippocampal CA3 region. These changes were significantly attenuated by
OPC-14117, which was administered as a single dose immediately following
trauma induction. The above results indicate that
oxygen free radicals are involved in
contusion-induced
edema formation, subsequent tissue damage and cognitive deficits. The
superoxide radical scavenger,
OPC-14117, has a powerful therapeutic potential for preventing secondary cell damage following
traumatic brain injury.