Objective To explore the neuroprotective effect and specific mechanism of ASI in protecting spinal cord ischemia-reperfusion injury (SCIRI) neurons. Methods A total of 60 male SD rats were randomly divided into 4 groups: Sham group, SCIRI group, SCIRI+ASI group and SCIRI+ASI+CC (AMPK inhibitor) group. The SCIRI+ASI group and SCIRI+ASI+CC group received intraperitoneal injection of ASI ［10 mg/(kg〖DK〗·d)］. The Sham group and SCIRI group were intraperitoneally injected with the same volume of physiological saline. The ASI (dissolved in physiological saline ［10 mg/(kg·d)］ was intraperitoneally injected for 3 days before SCIRI treatment, and the final dose was given 10 minutes before reperfusion. The CC (0.25mg/kg) was injected 10 minutes before reperfusion. This study used ligation of the distal descending aorta of the left subclavian artery and reperfusion after 14 minutes. After 24 hours, blood and spinal cord (L2-L5) samples were taken for morphological and biochemical examination. Results After SCIRI treatment, the rats exhibited motor dysfunction, increased cell apoptosis, increased malondialdehyde content, increased mitochondrial biogenesis, and dynamic balance disorders. After ASI intervention, adenosine monophosphate activated protein kinase (AMPK) was activated, and mitochondrial damage was improved. The oxidative stress was weakened and neuronal damage was partially recovered. The Compound C intervention significantly weakened the protective effect of ASI. Conclusion Oxidative stress and pyroptosis caused by mitochondrial damage is one of the important mechanisms of SCIRI neuronal damage. The ASI can activate AMPK to stabilize mitochondrial biogenesis and dynamic balance and reduce neuronal damage caused by oxidative stress and pyroptosis