title: [The expression of α-smooth muscle actin during the lung injury induced by hyperoxia].
abstract: 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 (FiO(2)) was 0.21] and hyperoxia exposure group (95%O(2)) according to random digits table. Eight rats in each group were randomly sacrificed at day 1, 7, 14 and 21.Pulmonary tissue remodeling was observed 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.
authors.affiliation: Department of Critical Care Medicine, Chongqing Medical University, Chongqing, China.
authors.forename: Yue-qiang
authors.initials: YQ
authors.lastname: Fu
authors.forename: Cheng-jun
authors.initials: CJ
authors.lastname: Liu
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Lan
authors.initials: L
authors.lastname: Hu
authors.forename: Zhong-yi
authors.initials: ZY
authors.lastname: Lu
authors.forename: Feng
authors.initials: F
authors.lastname: Xu
mesh_terms: D000199:Actins / Q000378:metabolism*; D000818:Animals; D018496:Hyperoxia / Q000150:complications / Q000378:metabolism*; D008168:Lung / Q000378:metabolism; D055370:Lung Injury / Q000209:etiology / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000199:Actins; C498862:Acta2 protein, rat