Objective To explore the role of coenzyme Q10 in protection of traumatic brain injury（TBI） and its potential mechanism. Methods Adult male C57BL/6 mice were randomly selected and a controlled cortical impact（CCI）was used to establish a mouse model. The mice were randomly divided into Sham group，TBI group， CoQ10 low⁃dosage group（LDG）and high⁃dosage group（HDG）. Expression levels of inflammatory cytokines TNF⁃α， IL⁃6，and IL⁃1β were detected by real⁃time PCR. Apoptosis⁃related protein expression of Bcl⁃2，Bax and c⁃Caspase⁃3 were detected by Western blot. And the mRNA and protein levels of GAP43 were measured by both real⁃time PCR and Western blot. The injury degree and recovery of neural function in each group was assessed by using modified neurological severity scores（mNSS）and Rotarod test. Results As compared with TBI group，expression levels of TNF⁃α，IL⁃6，and IL⁃1β were significantly decreased in LDG and HDG（P < 0.05）；Bcl⁃2 expression was signifi⁃ cantly increased，while levels of Bax and c⁃Caspase3 markedly decreased and Bcl⁃2/Bax ratio declined（P < 0.05） in LDG and HDG. mRNA and protein levels of GAP43 were elevated after treatment with CoQ（P < 0.05）. As com⁃ pared with TBI group，the mNSS scores significantly decrease in LDG and HDG on days 7 and 14 after TBI（P < 0.05）； whereas，the Rotarod test time was prolonged（P < 0.05）. Conclusions Coenzyme Q10 may play a protective role for the mice with traumatic brain injury through decreasing cell apoptosis and levels of inflammatory factors.