Spinal cord injury is a common form of trauma. Ginkgolide B can affect the function of the nervous system. This research established a rat spinal cord injury model to investigate the impact of ginkgolide B on spinal cord injury and its relationship with STAT1 signaling pathway. Spinal cord injury model was applied on rats according to the reference. The rats were randomly divided into sham operation group, spinal cord injury group, and ginkgolide B group. Inclined plate test and Basso Beattie Bresnahan (BBB) score were adopted for evaluation. Cell apoptosis was evaluated by TUNEL assay. Bcl-2, Bax, and p-STAT1 expressions were measured by Western blot. Ginkgolide B significantly reduced cell apoptosis induced by spinal cord injury at 12 h, 24 h, and 48 h (P<0.05). Bcl-2 increased, while Bax declined in spinal cord injury rat. Ginkgolide B treatment markedly decreased Bcl-2 level and elevated Bax expression (P<0.05). Cell number in the spinal gray matter obviously increased after ginkgolide B treatment for 12 h, 24 h, and 48 h compared with spinal cord injury group (P<0.05). Spinal cord injury enhanced STAT1 phosphorylation, whereas ginkgolide B declined STAT1 phosphorylation at 12 h, 24 h, and 48 h (P<0.05). Ginkgolide B significantly increased rat inclined plate test results and BBB score (P<0.05). Ginkgolide B showed protective role in spinal cord injury by affecting STAT1 signaling pathway.