Objective: To study the effect and molecular mechanisms of tanshinone IIA on neuronal apoptosis in the compressed spinal cord. Method: SD rats were selected as experimental animals and randomly divided into a sham-operated group (Sham group), a spinal cord compression injury group (SCI group), a tanshinone IIA group (TAN group), and an LY2904002 group (LY group). The spinal cord compression model was established by clamping the spinal cords with an arterial clamp. Tanshinone IIA was given in the TAN group, and tanshinone IIA combined with LY2904002 was given in the LY group. On the third day after the intervention, the rats' motor functions were evaluated, and the expressions of the apoptotic gene and the PI3K/AKT signal molecules in the compressed spinal cord were measured. Results: The BBB scores, the ramp angles, and the expressions of GSK-3 beta, Cyclin D1, Bcl-2, p-PI3K, and p-AKT in the compressed spinal cords of the SCI group were lower than they were in the Sham group, but the expressions of Caspase-9 and Caspase-3 in the compressed spinal cords were higher than they were in the Sham group; the BBB scores, the ramp angles, and the expressions of GSK-3 beta, Cyclin D1, Bcl-2, p-PI3K, and p-AKT in the compressed spinal cords of the TAN group were higher than they were in the Sham group, but the expressions of Caspase-9 and Caspase-3 in the compressed spinal cords were lower than they were in the SCI group; the BBB scores, the ramp angles, and the expressions of GSK-3 beta, Cyclin D1, Bcl-2, p-PI3K, and p-AKT in the compressed spinal cords of the LY group were lower than they were in the TAN group, but the expressions of Caspase-9 and Caspase-3 in the compressed spinal cords were higher than they were in the TAN group. Conclusion: Tanshinone IIA can inhibit cell apoptosis in compressed spinal cords by activating the PI3K/AKT signaling pathway and can alleviate the degree of spinal cord injury in rats with spinal cord compression.