title: Colchicine protects against hyperoxic lung injury in neonatal rats.
abstract: BACKGROUND
  Bronchopulmonary dysplasia (BPD) is characterized by inflammation, fibrosis and mucosal necrosis, which leads to emphysematous coalescence of alveoli.
  
  
  OBJECTIVE
  We tested whether prophylaxis with colchicine , an anti-inflammatory, antioxidant and antifibrotic drug, would decrease the severity of lung injury in an animal model of BPD.
  
  
  METHODS
  Twenty-five rat pups were divided into three groups: control (n = 8), hyperoxia (n = 7), and hyperoxia + colchicine (n = 10). The hyperoxia groups were exposed to >95% oxygen from day 1 to 10 of life. On day 10, the animals were sacrificed and the lungs were processed for histology and biochemical analysis. Lung morphology was assessed by the mean linear intercept (MLI), a measure of alveolar size. The degree of lung inflammation and antioxidant capacity were assessed by quantifying lung homogenate tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels.
  
  
  RESULTS
  Colchicine significantly decreased lung damage as determined by the MLI in the hyperoxia groups (p < 0.01). The median level of lung MDA was significantly higher in the hyperoxia group compared with the control group (p < 0.05) and the colchicine-treated group (p < 0.05). Lung homogenate SOD and GSH-Px activities in the colchicine-treated group were significantly higher than in the hyperoxia group (p < 0.05). Furthermore, colchicine-treated pups had lower lung homogenate TNF-α and IL-1β levels compared with the hyperoxia group (p < 0.05).
  
  
  CONCLUSIONS
  Colchicine has favorable effects on alveolarization as well as inflammation and oxidative stress markers in an animal model of BPD.
authors.affiliation: Division of Neonatology, Department of Pediatrics, Turgut Özal Medical Center, Inönü University School of Medicine, Malatya, Turkey. ramazanoz@yahoo.com.tr
authors.forename: Ramazan
authors.initials: R
authors.lastname: Ozdemir
authors.forename: Sadık
authors.initials: S
authors.lastname: Yurttutan
authors.forename: Beril
authors.initials: B
authors.lastname: Talim
authors.forename: Bülent
authors.initials: B
authors.lastname: Uysal
authors.forename: Omer
authors.initials: O
authors.lastname: Erdeve
authors.forename: Serife Suna
authors.initials: SS
authors.lastname: Oguz
authors.forename: Ugur
authors.initials: U
authors.lastname: Dilmen
mesh_terms: D055371:Acute Lung Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D000831:Animals, Newborn; D000833:Animals, Suckling; D000975:Antioxidants / Q000627:therapeutic use*; D003078:Colchicine / Q000627:therapeutic use*; D004195:Disease Models, Animal; D005260:Female; D005979:Glutathione Peroxidase / Q000032:analysis / Q000378:metabolism; D018496:Hyperoxia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D053583:Interleukin-1beta / Q000032:analysis / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D000975:Antioxidants; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003078:Colchicine