Objective: The aim of this study was to explore the value of a ketoglutarate dehydrogenase complex (alpha-KGDHC) activity in hypothermia treatment of acute brain injuries. Method: Ninety 8-week-old SD rats were randomly divided into three groups (n=30 each). The control group was normally raised. The other two groups underwent acute brain injuries. One group of rats underwent hypothermia treatment at 30-35 degrees C (treatment group), while the other group underwent conventional therapy (model group). Ten rats in each group were sacrificed before injury (T1), 5 days after injury (T2), and 10 days after injury (T3). Middle cerebral artery peak systolic velocity (Vs), pulse wave velocity (Wv) and brain injury markers were measured, including myelin basic protein (MBP), brain-derived neurotrophic factor (BDNF), S-100 protein (S-100B), and serum alpha-KGDHC expression levels. Pearson's correlation analysis of alpha-KGDHC, BDNF, and S-100B was performed. Result: At T1, T2, and T3, MBP and S-100B levels in the control group were significantly lower than those in the treatment and model groups (P<0.050). MBP and S-100B in the treatment group were significantly lower than those in the model group (P<0.050). As time went on, MBP and 5-100B decreased gradually (P<0.050). At T1, T2, and T3, expression levels of alpha-KGDHC and alpha-KGDHC activity in the control group were significantly higher than those in the treatment group and model group (P<0.050). Pearson's correlation analysis showed that BDNF was positively correlated with alpha-KGDHC activities at T1, T2, and T3 (r=0.863, 0.791, 0.682, P<0.050). There was a negative correlation between sloop and alpha-KGDHC activity at T1, T2, and T3 (r=-0.842, -0.941, 06-63, P<0.050). Conclusion: Mild hypothermia treatment of acute brain injuries in rats can effectively reduce brain damage and improve nerve repair ability. Monitoring the activity of alpha-KGDHC in patients can effectively assess the repair of brain damage in patients.