目的　探讨内质网应激在早产鼠高氧肺损伤中的作用。方法　48只新生早产Wistar大鼠在生后12 h随机分为对照组和高氧组，高氧组吸入95%的高浓度氧建立高氧肺损伤模型，对照组置于同一条件常压空气中。在处理后1、3、7 d分批断颈放血处死大鼠后取肺组织。每个时间点取动物8只，左肺制作石蜡切片，采用HE染色观察肺组织病理变化；免疫组织化学链霉菌抗生物素蛋白-过氧化物酶连结(SP)法检测内质网应激相关指标，内质网蛋白57(ERp57)、CCAAT增强子结合蛋白同源蛋白(CHOP)在肺组织中的表达；采用原位末端标记法(TUNEL)检测肺细胞凋亡情况。结果　高氧组肺组织呈典型的急性肺损伤改变。除了暴露3 d，其余时间点，高氧组ERp57和CHOP表达均高于对照组，差异有统计学意义(P<0.05)。随高氧暴露时间延长，高氧组ERp57表达呈增高趋势，差异有统计学意义(P<0.05)；但CHOP表达在各时间点差异无统计学意义(P>0.05)。肺组织细胞凋亡指数随时间延长呈渐升趋势，在暴露1 d、3 d、7 d之间的差异有统计学意义(P<0.01)；在各时间点，高氧组凋亡指数均高于对照组，差异有统计学意义(P均<0.01)。ERp57、CHOP表达与高氧组肺组织细胞凋亡指数呈显著正相关(P均<0.01)。结论　内质网应激启动的凋亡途径参与高氧肺损伤，并发挥重要作用。

　Objective　To explore the effects of endoplasmic reticulum (ER) stress in the hyperoxia-induced lung injury in premature rats. Methods Forty-eight premature Wistar rats were randomized into two groups 12 hours after birth: hyperoxia group (n=24) inhaled 95% oxygen and control group (n=24) inhaled air. Eight rats were sacrificed in each group on day 1, 3, 7 after the treatment and the left lungs were embedded. The pathological changes in the HE stained sections of lung tissues were observed. The expressions of ER related protein ERp57 and c/EBP homologous protein CHOP were detected by immuno histochemistry and the apoptosis of lung cells was detected by TUNEL analysis. Results The typical pathological characteristics of acute lung injury were observed in hyperoxia group. The expressions of ERp57 and CHOP were increased with the exposure time in hyperoxia group, and were significantly higher than in control group (P < 0.05). The apoptosis rate of lung cells in hyperoxia group was significantly higher than in control group (P < 0.01). There was significant positive correlation between cell apoptosis index and expressions of Erp57 and c/EBP homogeneous protein. Conclusions ER stress initiated apoptosis participates and plays an important role in the process of hyperoxia-induced lung injury in premature rats.