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机构地区:[1]中国医科大学附属盛京医院儿科,沈阳110004 [2]中国医科大学人事处,沈阳110001 [3]厦门市湖里区妇幼保健院,福建厦门361009
出 处:《实用儿科临床杂志》2009年第2期99-101,共3页Journal of Applied Clinical Pediatrics
摘 要:目的探讨新生大鼠持续吸入高体积分数氧(高氧)后肺组织病理学变化,以及肺组织Ⅰ型和Ⅳ型胶原mRNA表达的动态改变和在高氧致慢性肺疾病(CLD)发生中的作用。方法足月新生大鼠出生12h内,依据吸入氧体积分数的不同随机分为高氧组和空气对照组。分别于实验1、3、7、14、21d,从2组中抽取5只,水合氯醛麻醉后取肺组织制备石蜡切片;行HE染色镜下观察肺组织病理变化;应用原位杂交方法检测其肺组织Ⅰ型和Ⅳ型胶原mRNA的动态表达和定位。采用SPSS11.0软件进行统计学分析。结果高氧组早期出现炎性反应,7d出现肺泡发育阻滞,最终形成纤维化。原位杂交光镜下可见,Ⅰ型胶原在新生大鼠肺组织中主要表达于肺泡上皮细胞和血管内皮细胞;与对照组比较7d时在高氧组Ⅰ型胶原mRNA表达显著降低(P<0.05),14d时差异更为显著(P<0.01);Ⅳ型胶原在新生大鼠肺组织中主要表达在血管内皮细胞,各时间点上2组Ⅳ型胶原mRNA表达水平比较无明显差异(Pa>0.05)。结论持续吸入高氧可引起新生大鼠肺发育受阻和肺间质纤维化等,与CLD相似改变,而Ⅰ型和Ⅳ型胶原mRNA表达水平与其蛋白的沉积不平行,提示此2型胶原的调节可能不是以转录水平为主。Objective To explore the dynamic changes of collagen type Ⅰ and Ⅳ messenger ribonucleic acid(mRNA) expression in the lung tissue of neonatal rats after inhaling high concentration of oxygen and the role of collagen type Ⅰ and Ⅳ mRNA in chronic lung disease (CLD) induced by hyperoxia. Methods Full - term newborn rats were grouped according to inhale the concentration of oxygen into hyperoxia group and air control group after birth within 12 hours. Lung histological section at day 1,3,7,14 and 21 in 2 groups were prepared for hematoxylin - eosin staining and the detection of mRNA level of collagen type I and IV by in situ hybridization. The results were analyzed with SPSS 11.0 software. Results Compared with air control group,inflammation response was seen in early stage, the arrest of lung development was evident after 7 d of oxygen exposure, at last interstitial fibrosis. It was shown that the positive expression of collagen type Ⅰ was mainly in the alveolar epithelial cells and endothelial cells by in situ hybridization. The expression of collagen type Ⅰ mRNA was weakened compared to air group on 7 d ( P 〈 0.05 ) and 14 d of oxygen exposure ( P 〈 0.01 ). While for collagen type Ⅳ, the positive expression was mainly in the endothelial cells,whose mRNA expression showed no evident change between two groups on each time (Pa 〉 0.05 ). Conclusions Prolonged hyperoxia may cause the onset of arrested lung development and lung fibrosis, which are similar to the changes of chronic lung disease. The collagen type Ⅰ and Ⅳ mRNA expressions are not parallel to their protein contents, suggesting the main modulation of these collagens may be not at transcriptional level.
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