CAJ | 학술논문

目的探讨高氧暴露下大鼠肺损伤中肌成纤维细胞表面标志α-平滑肌肌动蛋白(α -SMA)的表达变化及意义.方法将64只3周龄SD大鼠按随机数字表法分为正常对照组(置于空气中,吸入氧浓度0.21)和高氧暴露组(置于玻璃氧舱中,95％氧),每组于高氧暴露1、7、14、21d随机处死8只大鼠.苏木素-伊红(HE)染色观察肺组织病理改变,免疫组化法观察α -SMA在肺组织中的表达与分布,蛋白质免疫印迹法( Western blotting)检测肺组织α-SMA表达.结果 HE染色发现,早期高氧肺损伤时肺组织以炎症水肿表现为主,后期则以间质纤维增生为主.免疫组化结果显示,正常对照组α -SMA在细支气管上皮、肺泡表面及肺泡间隔上表达极为微弱；高氧暴露后随时间的延长α-SMA在肺泡表面及肺泡间隔上表达逐渐增强,以21d时最为明显.Western blotting检测发现,与正常对照组相比,高氧暴露1d、7d时肺组织α-SMA表达无明显差异(1.02±0.12比1.00±0.13,1.05±0.14比0.99±0.12,均P＞0.05),高氧暴露14d、21d时α-SMA表达明显增强(1.27±0.21比1.05±0.15,2.26±0.28比1.05±0.14,P＜0.05和P＜0.01).结论大鼠高氧暴露后随时间延长,α-SMA在肺组织中的表达逐渐升高,肺纤维化逐渐加重,说明肌成纤维细胞在肺组织纤维化重构过程中起重要作用.
목적 탐토고양폭로하대서폐손상중기성섬유세포표면표지α-평활기기동단백(α -SMA)적표체변화급의의.방법 장64지3주령SD대서안수궤수자표법분위정상대조조(치우공기중,흡입양농도0.21)화고양폭로조(치우파리양창중,95％양),매조우고양폭로1、7、14、21d수궤처사8지대서.소목소-이홍(HE)염색관찰폐조직병리개변,면역조화법관찰α -SMA재폐조직중적표체여분포,단백질면역인적법( Western blotting)검측폐조직α-SMA표체.결과 HE염색발현,조기고양폐손상시폐조직이염증수종표현위주,후기칙이간질섬유증생위주.면역조화결과현시,정상대조조α -SMA재세지기관상피、폐포표면급폐포간격상표체겁위미약；고양폭로후수시간적연장α-SMA재폐포표면급폐포간격상표체축점증강,이21d시최위명현.Western blotting검측발현,여정상대조조상비,고양폭로1d、7d시폐조직α-SMA표체무명현차이(1.02±0.12비1.00±0.13,1.05±0.14비0.99±0.12,균P＞0.05),고양폭로14d、21d시α-SMA표체명현증강(1.27±0.21비1.05±0.15,2.26±0.28비1.05±0.14,P＜0.05화P＜0.01).결론 대서고양폭로후수시간연장,α-SMA재폐조직중적표체축점승고,폐섬유화축점가중,설명기성섬유세포재폐조직섬유화중구과정중기중요작용.
Objective To explore the expression of α-smooth muscle actin ( α -SMA ) during the lung injury induced by hyperoxia in infantile rats.Methods Sixty-four male Sprague-Dawley (SD) rats about 3 weeks were randomly assigned into normal control group which exposured to room air [fraction of inspired oxygen (FiO2) was 0.21 ]and hyperoxia exposure group (95％O2) according to random digits table.Eight rats in each group were randomly sacrificed at day 1,7,14 and 21.Pulmonary tissue remodeling was ohserved by hematoxylin-eosin ( HE ) staining.Immunohistochemistry method was performed to evaluate the expression of α-SMA in pulmonary tissue,further Western blotting was also made to determine the expression of α-SMA.Results The early histopathologic changes after HE were inflammation and edema in pulmonary tissue,while the later changes were interstitial hyperplasia and fibroblast proliferation.The expression of α-SMA was very slight in bronchial epithelium,alveolar epithelium and alveolar interstitium in normal control group,but increased with the time of hyperoxia exposure prolonged and peaked at 21st day.Western blotting detected that the expression of α-SMA after hyperoxia exposure for 1 day and 7 days in hyperoxia exposure group presented no difference compared with normal control group ( 1.02 ± 0.12 vs.1.00 ± 0.13,1.05 ± 0.14 vs.0.99 ± 0.12,both P＞0.05 ),but the expression of α-SMA after hyperoxia exposure for 14 days and 21 days was increased compared with normal control group ( 1.27 ± 0.21 vs.1.05 ± 0.15,2.26 ± 0.28 vs.1.05 ± 0.14,P＜0.05 and P＜0.01 ).Conclusions Pulmonary fibrosis remodeling was caused by hyperoxia exposure.The expression of α-SMA in pulmonary tissue in hyperoxia exposure groups obviously increased,and could play an important role in pulmonary fibrosis remodeling.