The change of myofibroblast distribution in hyperoxia induced bronchopulmonary dysplasia in newborn rats
陈宁, GAO Fei, 刘雪雁, 韩晓华, 蔡栩栩, 薛辛东
Abstract
陈宁, GAO Fei, 刘雪雁, 韩晓华, 蔡栩栩, 薛辛东
Abstract
Objective To investigate the expression of alpha-smooth muscle actin (α-SMA) and collagen Ⅰ in lung tissue of newborn rats with hyperoxia induced bronchopulmonary dysplasia(BPD) and to explore the relationship between the myofibroblast and BPD. Methods Neonatal rats were exposed to room air or 85% oxygen for 21 days. Six rats of both groups were sacrificed at day 1,3,7,14 and 21. The left lung tissues were fixed, the right lung tissues were stored at - 80 ℃. The pathologic changes of lung were observed under optical microscope. Distribution of α-SMA in the lung were determined by immonohistochemical method. The protein and mRNA levels of collagen Ⅰ were detected by ELISA and RT-PCR respectively. Results Prolonged exposure to hyperoxia could result in secondary septum decreasing, enlarging terminal air space and increased collagen deposition in lung tissue. In hyperoxia group,α-SMA expression increased significantly in smooth muscle,alveolar septa interstitium and the surface of alveolar on day 14 and 21. But in air group,α-SMA expressed mainly at the tip of the secondary septa except in smooth muscle. Collagen Ⅰ deposition increased with hyperoxia exposure time prolonged. There was positive correlation between the expression of α-SMA and collagen Ⅰ mRNA in the lung tissue of hyperoxia group. Conclusion The pathological changes of lung injury induced by hyperoxia exposure in newborn rats are consistent with BPD of newborn infant. Abnormality of myofibroblast distribution may play an important role in pathogenesis of BPD. Key words: Bronchopulmonary dysplasia ; Alpha-smooth muscle actin ; Myofibroblast ; Rat ;
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Objective To investigate the expression of alpha-smooth muscle actin (α-SMA) and collagen Ⅰ in lung tissue of newborn rats with hyperoxia induced bronchopulmonary dysplasia(BPD) and to explore the relationship between the myofibroblast and BPD. Methods Neonatal rats were exposed to room air or 85% oxygen for 21 days. Six rats of both groups were sacrificed at day 1,3,7,14 and 21. The left lung tissues were fixed, the right lung tissues were stored at - 80 ℃. The pathologic changes of lung were observed under optical microscope. Distribution of α-SMA in the lung were determined by immonohistochemical method. The protein and mRNA levels of collagen Ⅰ were detected by ELISA and RT-PCR respectively. Results Prolonged exposure to hyperoxia could result in secondary septum decreasing, enlarging terminal air space and increased collagen deposition in lung tissue. In hyperoxia group,α-SMA expression increased significantly in smooth muscle,alveolar septa interstitium and the surface of alveolar on day 14 and 21. But in air group,α-SMA expressed mainly at the tip of the secondary septa except in smooth muscle. Collagen Ⅰ deposition increased with hyperoxia exposure time prolonged. There was positive correlation between the expression of α-SMA and collagen Ⅰ mRNA in the lung tissue of hyperoxia group. Conclusion The pathological changes of lung injury induced by hyperoxia exposure in newborn rats are consistent with BPD of newborn infant. Abnormality of myofibroblast distribution may play an important role in pathogenesis of BPD. Key words: Bronchopulmonary dysplasia ; Alpha-smooth muscle actin ; Myofibroblast ; Rat ;
Key concepts: Hyperoxia, Bronchopulmonary dysplasia, Myofibroblast, Medicine, Lung, Pathology, Pathogenesis, Internal medicine