CAJ | 학술논문

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.
목적 탐토결양유도사렬원인자(HIMF)재소서지기관폐발육불량(BPD)모형중적표체급의의.방법 32지신생곤명소서수궤분위대조조(n=16)、고양폭로조(n=16),분별치우정상공기(21%,O2)급양상(85%,O2)중,우폭로후제7、14、21、28천매조수궤선취4지,채용소목소-이홍(HE)염색관찰폐조직형태학개변,운용실시정량역전록-취합매련반응(RT-PCR)、Western blot방법검측폐조직중HIMF mRNA화단백표체수평.결과 대조조폐포축점발육성숙,대소균균,폐간질변박;고양폭로조폐포격증후、폐포융합,방사상폐포계수감소31.1%～65.3%;여대조조비교,고양폭로7、14、21 d후폐조직HIMF mRNA화단백수평분별증고2.435～2.528배(P<0.05)、2.45～5.42배(P<0.05),이고양폭로28 d후분별하조52.81%(P<0.05)、74.60%(P<0.05).결론 성공건립소서BPD모형,HIMF기인표체이상가능삼여BPD적발생、발전과정.
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.