Ginkgolide A attenuated apoptosis via inhibition of oxidative stress in mice with traumatic brain injury.

ABSTRACT

Traumatic brain injury (TBI) is the main cause of death among young adults and the main cause of mortality and disability for all ages groups worldwide. Ginkgolides terpenoid compounds unique to Ginkgo biloba, which have protective effects on cardiovascular and cerebrovascular diseases. The aim of this study is to investigate whether ginkgolide A (GA) can improve TBI in mice and whether it can alleviate cell apoptosis in the brain of TBI mice by reducing oxidative stress. Mice received TBI and GA administration for 7 days. Neurological deficits were monitored and brain tissues were examined for molecular pathological markers. TBI mice had more severer neurobehavioral deficits compared with sham group, which could be improved by administration of GA. GA administration improveed Modified Neurological Severity Scale (mNSS) scores, Grid-Walking test and Rotarod test of TBI mice. The apoptosis increased in TBI mice, and reduced after GA treatment. The biomarkers of oxidative stress 8-OHdG and malondialdehyde (MDA) in the brain of TBI mice increased, while SOD reduced. These changes were reversed after GA administration. These outcomes showed that GA could raise neurobehavioral deficiency of TBI mice. GA treatment could attenuate apoptosis in TBI mice by reducing oxidative stress.