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作 者:全裕凤[1] 郑明慈[2] 张华[1] 张培林[1] 张红[1]
机构地区:[1]桂林医学院附属医院新生儿科,广西桂林541001 [2]桂林医学院围产医学研究室,广西桂林541001
出 处:《中国当代儿科杂志》2011年第7期577-580,共4页Chinese Journal of Contemporary Pediatrics
基 金:广西科技厅科技攻关基金(0472002-35);广西卫生厅医药卫生基金(Z2001061)
摘 要:目的探讨血红素加氧酶-1(HO-1)与诱导型一氧化氮合酶(iNOS)在高氧肺损伤大鼠中的表达及作用。方法将3日龄早产Sprague-Dawley大鼠64只随机分为高氧组、空气组(每组32只),于实验3 d及7 d时,分别检测空气组和高氧组肺组织HO-1活性、肺泡灌洗液中NO、肺组织病理学改变及HO-1、iNOS在肺内的分布和表达(免疫组织化学方法)。结果 3 d、7 d高氧组存在明显急性肺炎症性改变,iNOS在中性粒细胞的表达、灌洗液中NO含量明显高于空气组(P均<0.01),且7 d高氧组高于3 d高氧组(P<0.05);3 d、7 d时高氧组巨噬细胞HO-1表达高于空气组(分别P<0.05,P<0.01),且7 d高氧组显著高于3 d高氧组(P<0.01)。结论 HO-1与iNOS在高氧肺损伤大鼠中的表达是增高的,HO-1与iNOS均可能参与了高氧肺损伤。Objective To study the expression and the role of heme oxygenase-1(HO-1) and inducible nitric oxide synthase(iNOS) in preterm rats with hyperoxia-induced lung injuries.Methods Sixty-four three-day-old preterm Sprague-Dawley rats were randomly assigned to a hyperoxia group(90% oxygen exposure) and a control group(room air exposure),with 32 rats in each group.After 3 days or 7 days of exposure,the lung activity of HO-1 and nitric oxide(NO) contents in bronchoalveolar lavage fluid(BALF),pulmonary histopathologic changes,and the cellular distribution and expression of HO-1 and iNOS in the lungs were measured.Results After 3 days and 7 days of exposure,the hyperoxia group showed acute lung injuries characterized by the presence of hyperaemia,red cell extravasation and inflammatory infiltration.The NO contents in BALF and the iNOS expression in the lungs increased significantly in the hyperoxia group compared with those in the control group 3 and 7 days after exposure.The expression of HO-1 in macrophages in the lungs increased significantly in the hyperoxia group compared with that in the control group 3 and 7 days after exposure.The NO contents in BALF and the iNOS and HO-1 expression in the lungs increased significantly 7 days after hyperoxia exposure compared with 3 days after hyperoxia exposure.Conclusions iNOS and HO-1 levels in the lungs increase in preterm rats with hyperoxia-induced lung injuries,suggesting that iNOS and HO-1 may play roles in hyperoxia-induced pulmonary injuries.
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