【Abstract】 Objective To investigate the effect and mechanism of neural cell apoptosis of acute spinal cord injury (ASCI) rats through regulating TNFR/RIPK signaling pathway. Methods 160 male SD rats were randomly divided into blank control group, sham operation group, model group, and Nec1 group. Each group was divided into four subgroups according to time points: 12h, 24h, 3d, and 7d. The sham operation group (normal saline): spinal cord was exposed without injury. Model group (normal saline) and Nec1 group (1μl/kg Nec1): spinal cord was injured by artery clamp methods and the wound was sewn up. The blank control group received no treatment. The medication was once a day, and lasted for 12h, 24h, 3d, 7d respectively. After medication, the BBB score was performed. The spinal cord of 10 rats administered with 7d were used for HE staining, Nissl staining, propidium iodide (PI) staining, Tunel staining; Another spinal cord of 10 rats administered with 7d were used for the detection of RIP1, RIP3 and Bcl2 protein expression levels by Western Blot. Results The BBB score of three groups in a descending order was blank control group sham operation group, Nec1 group and model group (P＜005). Neuronal manifestations of each group at the postmodeling 7d: the percentage of spinal cord necrosis, cavitation, massive inflammatory cell infiltration, and necrotic area of the model group was higher than that of the sham operation group and blank control group (P＜005). The percentage of finegrained Nissl body, neurons of reduced, light staining and disordered, and increased necrotic apoptotic cells was high. The number of PI staining cells, Tunel positive cells, number of apoptotic bodies, and RIPK1, RIPK3 and Bcl2 protein expression in the model group were significantly higher than those in the sham operation group and blank control group (P＜005). At the post 7d of Nec1medication, the above changes in the Nec1 group were ameliorated (P＜005). The number of PIstained cells, the number of apoptotic bodies, and the expression levels of RIPK1 and RIPK3 proteins in the Nec1 group were significantly lower than those in the model group (P＜005). The expression of Bcl2 protein in Nec1 group was significantly higher than that in the model group (P＜005). Conclusion The necroptotic inhibitor Nec1 can inhibit necrotizing apoptosis by inhibiting TNFR/RIPK signaling pathway, which indicates to downregulate RIPK1, RIPK3, upregulate the expression of Bcl2, reduce inflammatory infiltration, reduce the number of peripheral neurons in injury, ameliorate the neuronal function, and improve the survival rate of damaged neurons and glial cells.