Objective：To investigate the expression of SPOCK2 gene in hyperoxia-induced bronchopulmonary dysplasia（BPD）models of neonatal rats. Methods：BPD models were induced by 85% O2 exposure. Newborn SD rats were randomly divided into the air group and the hyperoxia（85% oxygen）group. The pathological changes of pulmonary tissues were observed by hematoxylin-eosin（HE）staining. The expressions of SPOCK2 mRNA were detected by real-time quantitative PCR. The expression of SPOCK2 protein was detected by immunohistochemistry. Meanwhile，A549 lung epithelial cells were stimulated by hyperoxia in vitro and the expression levels of SPOCK2 mRNA were detected by qPCR. Results：BPD neonatal rat model was successfully constructed. The pathological changes of BPD were found in the pulmonary tissues of the model group by HE staining. The value of pulmonary radical alveolar counts（RAC）in the model group was significantly lower than that of the control group at 10 d and 14 d after birth（P < 0.05）. As shown with immunohistochemistry，the expression of SPOCK2 protein in the lung tissues of rats in the control group was higher than that in the model group，especially at 10 d and 14 d after birth. The expression of SPOCK2 mRNA in the lung tissues of rats in the control group was higher than that in the model group，which reached its peak on 18 d after birth and decreased in adulthood. Compared with the control group，the expression of SPOCK2 mRNA in the model group decreased. There were significant difterences befween two groups at 10 d and 14 d after birth（P < 0.05）. The expression of A549 mRNA in the model A549 cells was higher than that in the control（P < 0.05）. Conclusion：SPOCK2 gene may be involved in pulmonary development process，and may protect lung tissue during hyperoxia stimulation.