摘要
目的 探讨缺氧诱导丝裂原因子(HIMF)在小鼠支气管肺发育不良(BPD)模型中的表达及意义.方法 32只新生昆明小鼠随机分为对照组(n=16)、高氧暴露组(n=16),分别置于正常空气(21%,O2)及氧箱(85%,O2)中,于暴露后第7、14、21、28天每组随机选取4只,采用苏木素-伊红(HE)染色观察肺组织形态学改变,运用实时定量逆转录-聚合酶链反应(RT-PCR)、Western blot方法检测肺组织中HIMF mRNA和蛋白表达水平.结果 对照组肺泡逐渐发育成熟,大小均匀,肺间质变薄 高氧暴露组肺泡隔增厚、肺泡融合,放射状肺泡计数减少31.1%~65.3% 与对照组比较,高氧暴露7、14、21 d后肺组织HIMF mRNA和蛋白水平分别增高2.435~2.528倍(P〈0.05)、2.45~5.42倍(P〈0.05),而高氧暴露28 d后分别下调52.81%(P〈0.05)、74.60%(P〈0.05).结论 成功建立小鼠BPD模型,HIMF基因表达异常可能参与BPD的发生、发展过程.
Objective To study the expression of hypoxia-induced mitogenic factor (HIMF) in mouse bronchopulmonary dysplasia ( BPD) model and its significance. Methods Thirty-two Kunming neonatal mice were randomly divided into normoxia exposure group (21% 02,n=16) and hyperoxia exposure group (85% O2,n=16). After exposure for 7, 14, 21 and 28 days, HE staining was applied to observe the morphological changes of lung tissues. The mRNA and protein levels of HIMF were detected by real-time reverse transcription-polymerase chain reaction ( RT-PCR) and Western blotting, respectively. Results In normoxia exposure group, the alveoli was gradually mature and well-distributed, with thin interstitial tissue. However, in hyperoxia exposure group, the increased septa] wall thickness and alveolar fusion were observed, and the radical alveolar count was decreased by 31.1%-65.3%. As compared with normoxia exposure group, the mRNA and protein levels of HIMF were enhanced by 2.435-2.528 times (P〈0.05) and 2.45-5.42 times (P〈0.05) at the 7th, 14th and 21st day after exposure, but decreased by 52. 81 % (P〈0. 05) and 74. 60% at the 28th day after exposure. Conclusion The mouse BPD model was successfully established, and HIMF may participate in the pathogenesis of BPD.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2010年第7期943-945,I0003,共4页
Chinese Journal of Experimental Surgery
基金
基金项目:国家自然科学基金资助项目(30200284、30600278、30772359)
教育部新世纪优秀人才支持计划资助项目(NCET-06-0641)
教育部留学回国人员科研启动基金资助项目(2008889)