Objective To investigate the mechanism of JAK-STAT after spinal cord injury. Methods Thirty Sprague Dawley rats were randomly divided into normal saline group and JAK stat inhibitor group, 15 rats in each group. Saline group was injected intraperitoneally after spinal cord injury, and JAK stat inhibitor group was injected intraperitoneally after spinal cord injury. The motor dysfunction score and spinal cord injury behavior score (BBB score) of the two groups after treatment were observed. The pathological changes of spinal cord injury in the two groups were detected by HE staining. The proliferation and expression of Ki67 were detected by immunohistochemical staining. The nuclear apoptosis was detected by immunofluorescence, and the apoptosis was detected by flow cytometry. Results There was no significant difference in the scores of motor dysfunction between the two groups (P＞0.05), but the BBB score of JAK stat inhibitor group was better than that of normal saline group (P＜0.05). The results of Ki 67 immunohistochemistry showed that the proliferation of JAK stat inhibitor group was significantly lower than that of normal saline group (P＜0.05). Flow cytometry showed that the number of apoptotic cells in JAK stat inhibitor group was significantly more than that in saline group (P＜0.05). Conclusion Inhibitors of the JAKStat signaling pathway alleviates spinal cord injury by reducing cell proliferation and increasing apoptosis.