〔Abstract〕 Objective To investigate the neurobehavioral effects of long-term mild hypothermia(MHT) combined with compound porcine cerebroside and ganglioside injection(CPCGI)after traumatic brain injury(TBI) in rats and its mechanism. Methods 36 healthy adult male SD rats were randomly divided into model group, MHT group, CPCGI group and MHT+CPCGI group. The TBI model was prepared using an electronically controlled cortical injury device. The rats in model group received an intraperitoneal injection of an equal amount of normal saline(NS, 2 ml/kg) and were treated at room temperature(37 ℃) for 48 hours. The rats in MHT group received an intraperitoneal injection of an equal amount of NS and were treated at a slightly low temperature(33.0±1.0) ℃ for 48 hours. The rats in CPCGI group received an intraperitoneal injection of an equal amount of CPCGI(0.6 ml/kg) and were treated at room temperature for 48 hours. The rats in MHT+CPCGI group received an intraperitoneal injection of an equal amount of CPCGI and were treated at a slightly low temperature for 48 hours. The sensorimotor function of rats was evaluated by modified Neurological Severity Score(mNSS). The motor and spatial memory abilities of rats were detected by Morris water maze test, and the motor function of rats was evaluated by beam walking test(BWT) and inclined-grid climbing test. The number of neurons in hippocampus was observed by Nissl staining and immunofluorescence was used to detect the expression of doublecortin(DCX) and neuronal nuclear antigen antibody(NeuN). Western blot was used to observe the protein expression of B-cell lymphoma-2(Bcl-2), Bcl-2 associated X protein(Bax) and cysteine proteinase-3(Caspase-3). Results Compared with MHT group and CPCGI group, MHT+CPCGI group had a lower mNNS score, shorter escape latency, higher times across the platform and the percentage of time in the target quadrant, higher BWT score and larger climbing angle, increased numbers of neurons, DCX and NeuN positive cells, increased Bcl-2 expression and decreased expression of Bax and Caspase-3.(P<0.05). Conclusion Long-term mild hypothermia combined with CPCGI can effectively improve the neurological deficits of TBI rats by promoting nerve regeneration and inhibiting cell apoptosis, and provide potential strategies and basis for the clinical treatment of TBI.