Akademik Veri Yönetim Sistemi
NEONATOLOGY, cilt.102, sa.4, ss.265-269, 2012 (SCI-Expanded)
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-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), malondialde-hyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. Results: Colchicine significantly decreased lung damage as determined by the MLI in the c 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-alpha and IL-1 beta 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. Copyright (C) 2012 S. Karger AG, Basel