Objective To investigate the effects of S1P on Caspase-3, ERK and pulmonary artery smooth muscle cells in COPD rats. Methods Sixty COPD rats were divided into control group, COPD group and S1P group. Right ventricular systolic pressure and right ventricular hypertrophy index were compared among the three groups. Pathological changes of lung tissue were compared by HE staining. Apoptosis of pulmonary artery smooth muscle cells was detected by TUNEL. The expression of Caspase-3 and ERK protein in COPD rats was detected by protein imprinting. Results The values of fev0.3/fvc and cdyn in COPD group were significantly lower than those in sham group, and the values of RI were higher than those in sham group (P＜0.05). After intervention, the values of fev0.3/fvc and cdyn in S1P group were significantly increased, and the values of RI were significantly decreased (P＜0.05). Compared with the control group, the RVSP value and RVMI of COPD group were significantly increased (P＜0.05). After intervention, the RVSP value and RVMI of S1P group were significantly lower than those of COPD group (P＜0.05). Compared with the control group, the morphology of lung tissue in COPD group was significantly deteriorated, and a large number of apoptosis of pulmonary artery smooth muscle cells occurred; after intervention, the lung tissue of S1P group was significantly improved, and the apoptosis index of pulmonary artery smooth muscle cells was significantly inhibited compared with COPD group (P＜0.05). Protein comparison showed that compared with the control group, the expression of caspase-3 protein in COPD group was significantly increased, and the expression of p-ERK protein was significantly decreased (P＜0.05). Compared with COPD group, the expression of caspase-3 protein in S1P group was significantly inhibited, and the expression of p-ERK protein was significantly increased (P＜0.05).Conclusion S1P can inhibit the expression of Caspase-3, activate the expression of ERK, and promote the apoptosis of pulmonary artery smooth muscle cells.