Objective To explore the correlation between the changes of mitochondrial DNA (mtDNA) copy number of peripheral blood leukocytes and the degree of neurological impairment after traumatic brain injury (TBI).Methods A total of 40 Sprague Dawley rats were randomly divided into 4 groups:control group (n=10),mild TBI group (n=10),moderate TBI group (n=10) and severe TBI group (n=10).The cortical impact injury method to construct TBI rat model of different damage degree.The neurological score (mNSS,screen test,open field test) after TBI 24 h,48 h,72 h was performed and the orbital venous plexus blood genomic DNA was extracted.The real-time PCR method to measure the relative mitochondrial DNA copy number.After the experiment,the rats were euthanized,and the brain tissue was stained with hematoxylin-eosin staining(HE).Results There were significant differences in the HE staining findings of brain tissue pathology (P＜ 0.05).Each group of rats with brain injury after peripheral blood mtDNA copy number in 24 h (9.63±3.62,P＜0.05) and 48 h (9.80±3.58,P＜0.05) increased,began to decline at 72 h (4.97±2.68,P＜0.05).The rats mNSS scores were related with the mtDNA copy number after TBI 24 h (r=0.578,P＜0.05) and 48 h (r=0.559,P＜0.05),and not related to TBI 72 h (r=0.487,P＞0.05).The rats screen test scores were related with the mtDNA copy number after TBI 24 h (r=0.573,P＜0.05) and 48 h (r =0.501,P＜0.05),and not related to TBI 72 h (r=0.273,P＞0.05).The rats level scores of open field test were negatively correlated with the mtDNA copy number after TBI24 h (r=-0.662,P＜0.05) and 48 h (r=-0.507,P＜0.05),and not negatively correlated to TBI 72 h (r=-0.410,P＞0.05).The rats vertical scores of open field test were negatively correlated with the mtDNA copy number after TBI 24 h (r=-0.662,P＜0.05)and 48 h (r =-0.607,P＜ 0.05),and not negatively correlated to TBI 72 h (r =-0.141,P＞ 0.05).Conclusion TBI is related with the copy of early peripheral white blood cell number and mtDNA of rat nerve function damage,and mtDNA copy number of peripheral white blood cell may become a clinical evaluation of TBI neural function damage degree of a potential biomarker.