Objective：To investigate the effects and underlying mechanism of cryptotanshinone（CTS）on pulmonary fibrosis in rats with hyperoxia-induced bronchopulmonary dysplasia（BPD）. Methods：50 newborn male Sprague-Dawley rats were randomly divided into air group，hyperoxia group，low-dose CTS（7.5 mg/kg）group，medium-dose CTS（15.0 mg/kg）group and high-dose CTS（30 mg/kg） group. Rats in hyperoxia and three CTS treatment groups were exposed to 95% oxygen（O₂）for 7 d after birth，and the air group were exposed to a room environment（21% O₂）. 7 days later，all rats were euthanized. The alveolar morphology and lung fibrosis were evaluated using hematoxylin-eosin（HE）staining and Masson staining. The mRNA levels of transforming growth factor beta1（TGF-β1） and alpha-smooth muscle actin（α-SMA）were detected by RT-qPCR. The protein expression of cell signaling molecules small mother against decapentaplegic（Smad）2/3 and p -Smad2/3 was detected by Western blot. In vitro experiments：Human fetal lung fibroblasts （HFL-1）cells were selected and divided into air group，hyperoxia group and CTS intervention group according to the culture conditions. The air group was cultured under conventional conditions，while the hyperoxia and intervention groups were incubated in a 95% O₂ incubator for 24 h. 10 μmol/L CTS was added to the intervention group. Cell viability was measured by CCK-8 assay，and protein expression of TGF-β1，α-SMA，p-Smad2/3 and Smad2/3 were detected by Western blot. Results：Compared with the control group，rats in the hyperoxia group had disorderd alveolar morphology，widened alveolar septa，decreased RAC values and increased fibrosis scores（P < 0.05）；increased the mRNA levels of TGF-β1 and α-SMA（P < 0.05）；and up-regulated p-Smad2/3 expression（P < 0.05）. Different doses of CTS could improve the above indicators（P < 0.05）. Meanwhile，CTS also reduced TGF-β1，α-SMA，p-Smad2/ 3，and Smad2/3 protein expression levels in HFL-1 cells after hyperoxia（P < 0.05）. Conclusion：CTS ameliorates the fibrotic process of hyperoxia-induced lung injury via the TGF-β/Smad pathway.