Expression Of High Mobility Group Protein-b1 And Alpha-smooth Muscle Actin In Hyperoxia Exposure Induced Brochopulmonary Dysplasia Mice

Objective:To investigate the effect of HMGB1 (High mobility group proyeion-B1)andα-SMA ( Alpha-smooth muscle actin ) expression in newborn mouse with moderate hyperoxic exposure and the role of HMGB1 in the mechanism of BPD ( Bronchopulmonary dysplasia ).Methods :⑴C57BL/6 mice were randomly divided into a BPD group and a control group. BPD model was established by exposure to 60% O2 in the neonatal period of C57BL/6 mice. Mice exposesd to air were used as control groups, with 12 animals in each group on repeated experiments.⑵The pathology of pulmonary tissure was detected by HE stain .⑶The pathology of pulmonary tissure was detected by radical alveolar counts (RAC) .⑷The expressions of HMGB1 andα-SMA protein in lung were detected by immunofluorescence . ⑸The expressions of HMGB1 andα-SMA mRNA by real-time fluorescent quantitation PCR.Results:⑴In BPD groups, lungs developed decreased alveolar septation, swelled alveolar epithelium, stroma edema, interstitial fibrosis and developmental lag compared with control groups.⑵These changes became more obviously with more prolonged hyperoxia exposure.⑶The expression of HMGB1 protein after 7 and 14 days of exposure increased significantly in the hyperxia groups compared with control groups.⑷The expression of HMGB1 mRNA was also higher after 7 and 14 days of exposure. Bothα-SMA protein and mRNA level increased with increasing hyperoxia exposure time.Conclusions:⑴Hyperoxia caused progressive addition in lung HMGB1 andα-SMA expression as well as abnormalitilies of lung structures, including decreased grouth and impaired alveolarization. These histologic changes are similar to those of BPD.⑵There is a relationship between and increasing expression of HMGB1 and activatingα-SMA.