Abstract: Object To investigate the expression of endoplasmic reticulum stress-related protein GRP78 and caspase-12 in the lungs of bronchopulmonary dysplasis (BPD) rats. Methods Hyperoxia-induced preterm rat model of BPD was established. Forty-eight premature Sprague-Dawley rats were randomly divided into hyperoxia group and air group. The hyperoxia group was continually exposed to hyperoxia(85%) while the air group in room air. Lung tissues were obtained at 7, 14 and 21 days after exposing to either room air or hyperoxia. The changes of pulmonary histopathology were observed by hematoxylin-eosin (HE) staining and radical alveolar count (RAC). Apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL). The expressions of GRP78 and caspase-12 mRNA and protein levels were detected by real-time quantitative RT-PCR and western blot respectively. Results The lung of hyperoxia premature rats showed simple alveolar structure, fewer and larger alveoli, which shares morphologic similarities to BPD. Compared with the air group, hyperoxia exposure resulted in lower RAC and significant apoptosis. In addition, the expression levels of GRP78 and caspase-12 mRNA and protein increased significantly (P<0.01) and had a up-regulated trend. Conclusion The increased expression of GRP78 and caspase-12 may be involved in the pathogenesis of BPD.

Key words: GRP78, caspase-12, hyperoxia, bronchopulmonary dysplasis