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Neurons in the central nervous system (CNS) rarely regenerate after spinal cord injury (SCI) in adult mammals; this leads to permanently damaged sensory and motor function. However, the mechanism underlying neuronal apoptosis limits SCI is unclear. Here, we predicted the proteins and pathways that might be affected by syringaresinol by establishing a molecular docking model to determine ubiquitination factor E4B (UBE4B; ubiquitin chain assembly factor) binding to syringaresinol or proteins. We incubated SH-SY5Y cells with glutamate followed by syringaresinol and evaluated related protein expression. The AKT pathway and the expression of apoptosis-related proteins B-cell lymphoma 2 (BCL-2) and BCL-2-associated X protein were evaluated in SH-SY5Y cells incubated with syringaresinol. We detected UBE4B expression using Western blotting and reverse transcription quantitative polymerase chain reaction （RT-qPCR and evaluated recovery in rat SCI models using the Basso-Beattie-Bresnahan (BBB) rating scale and inclined plate tests. We assessed syringaresinol effects in rat SCI models by immunohistochemically staining for Neuron Nuclei (NeuN), ionized calcium-binding adapter molecule 1(IBA1), and Adenomatous Polyposis Coli (CC-1). Syringaresinin can bind to the U-box domain of UBE4B, which may degrade AKT inhibitory proteins PTEN, PP2A and other proteins to achieve the actual effect of UBE4B-ubiquitination. Syringaresinol accelerated recovery in a rat model of SCI by improving the pathological structure of injured spinal cord segments, increasing remyelination, and reducing inflammation via a phenomenon that substantially improved the BBB score. Syringaresinol may phosphorylated AKT and promoted its activation via UBE4B overexpression that reduced neuronal apoptosis, inhibited chronic inflammation, and accelerated myelination in the CNS.