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目的观察血红素加氧酶-1(HO-1)在高体积分数氧(高氧)暴露早产大鼠肺组织中的表达及活性变化,探讨HO-1在早产大鼠高氧肺损伤中的作用。方法将3日龄早产SD大鼠28只随机分为高氧组、空气组(每组14只),于实验第3、7天分别用半定量反转录-聚合酶链反应法和免疫组织化学法检测各组早产大鼠肺组织HO-1 mRNA表达水平和HO-1蛋白在肺组织的分布和表达水平,并测定HO-1的活性。采用SPSS 12.0软件进行统计学分析。结果实验第3天,空气组早产大鼠肺组织HO-1 mRNA(0.17±0.08)、HO-1蛋白(7.23±4.63)均有微弱表达,HO-1活性为(4.32±1.57)nmol/(mg.h);高氧组早产大鼠肺组织HO-1mRNA(0.72±0.33)表达明显高于空气组(Pa<0.01),HO-1蛋白(18.54±6.55)仅在巨噬细胞表达弱阳性,HO-1活性明显增加(6.14±1.62)nmol/(mg.h),二者均明显高于空气组(Pa<0.05)。实验第7天,各组早产大鼠肺组织HO-1 mRNA均未见表达,高氧组早产大鼠肺组织HO-1蛋白表达及活性均显著高于空气组[(51.24±18.32)vs(4.11±1.82),(32.38±5.46)nmol/(mg.h)vs(5.75±1.87)nmol/(mg.h)Pa<0.01]。结论HO-1可能参与了早产大鼠高氧肺损伤的过程。
Objective To observe the expression and activity of heme oxygenase-1 (HO-1) in lung tissue of premature rats with high volume fraction of oxygen (hyperoxia) exposure and to explore the role of HO-1 in hyperoxia-induced lung injury in premature rats effect. Methods 28 SD 3-day-old preterm rats were randomly divided into hyperoxia group and air group (14 in each group). On the 3rd and 7th days of the experiment, they were respectively treated by semi-quantitative reverse transcription-polymerase chain reaction and immunohistochemistry The expression of HO-1 mRNA and the expression of HO-1 protein in the lung tissue and the activity of HO-1 in lung of preterm rats were detected by chemical methods. SPSS 12.0 software was used for statistical analysis. Results On the third day of experiment, HO-1 mRNA (HO-1 mRNA, HO-1 protein, 7.23 ± 4.63, (0.72 ± 0.33) in lungs of premature rats in hyperoxia group were significantly higher than those in air group (P0.01). HO-1 protein (18.54 ± 6.55) was only weakly expressed in macrophages , HO-1 activity increased significantly (6.14 ± 1.62) nmol / (mg.h), both of which were significantly higher than those of air group (Pa0.05). On the 7th day of experiment, the expression of HO-1 mRNA in the lung tissue of premature rats in hyperoxia group was significantly higher than that in air group [(51.24 ± 18.32) vs ( 4.11 ± 1.82, (32.38 ± 5.46) nmol / (mg.h) vs (5.75 ± 1.87) nmol / (mg.h) Pa <0.01]. Conclusion HO-1 may be involved in the process of hyperoxia-induced lung injury in preterm rats.