中文摘要：

目的检测高迁移率族群蛋白B1（HMGB1）和α-平滑肌肌动蛋白（α-SMA）在中浓度高氧（60%O2）暴露新生小鼠肺组织损伤模型肺中的表达水平,探讨HMGB1在支气管肺发育不良（BPD）发病机制中的作用。方法新生足月C57BL/6小鼠随机分为氧处理组和空白对照组,制备中浓度高氧致新生鼠BPD模型,应用HE染色、放射性肺泡计数、免疫荧光和实时荧光定量-PCR技术观察生后第3、7、14天肺组织病理改变,HMGB1和α-SMA的蛋白及mRNA表达水平。结果氧处理组随时间推移,出现肺泡上皮肿胀,肺泡壁增厚,间质水肿,炎症细胞浸润,胶原样物质产生,较空白对照组明显发育迟滞。氧处理组HMGB1蛋白和mRNA在第7、14天时表达均强于相应空白对照组（P〈0.05）。氧处理组α-SMA蛋白和mRNA在第3、7、14天表达均强于相应空白对照组（P〈0.05）。HMGB1与α-SMA表达呈线性关系（P〈0.05）。结论在600 ml/L氧暴露所致BPD中,HMGB1和α-SMA表达增加。BPD的病理过程可能与HMGB1表达增加及α-SMA活化有关。

英文摘要：

Objective To investigate the expressions of HMGB1 and α-SMA in the lung of newborn mouse model with moderate hyperoxic exposure and the role of HMGB1 in the mechanism of BPD.Methods New term C57BL/6 mice were randomly divided into BPD group and control group.BPD model was established by exposure to 60% O2 in the neonatal period of C57BL/6 mice.The pathology of pulmonary tissue was detected by HE stain and radical alveolar counts（RAC）.The expressions of HMGB1 and α-SMA protein in lung were detected by immunofluorescence and the expressions of HMGB1 and α-SMA mRNA by real-time fluorescent quantitation PCR.Results In BPD groups,lungs developed thickened alveolar septum,swelled alveolar epithelium,interstitial edema and fibrosis and developmental lag compared with control groups.These changes became more obvious with more prolonged hyperoxia exposure.There is no significance of both HMGB1 protein and mRNA between the 3-day BPD group and controls.The expression of HMGB1 protein after 7 and 14 days of exposure increased significantly in the hyperoxia group compared with controls.The expression of HMGB1 mRNA was also higher after 7 and 14 days of exposure.Both α-SMA protein and mRNA level increased with increasing hyperoxia exposure time and kept linear relationship.Conclusions Both of the HMGB1 protein and mRNA increased in the BPD with hyperoxic exposure（600 ml/L）.The pathological process of BPD may be concerned with increased expression of HMGB1 and activated α-SMA.