检索结果-南通市图书馆

prenatal glucocorticoid contributed to rat lung dysplasia is related to asymmetric dimethylarginine/nitric oxide pathway

引用

Science Bulletin 2015年第16期60卷 1416-1425页

作者： Yu-Chieh Chen Li-Tung Huang You-Lin Tain Chih-Cheng Chen Jiunn-Ming Sheen Mao-Meng Tiao Chih-Min Tsai Ho-Chang Kuo Chao-Cheng Huang Kow-Aung ChangDepartment of Anesthesiology Chang Gung Memorial Hospital-Kaohsiung Medical Center Graduate Institute of Clinical Medical Science Chang Gung University College of Medicine Hong-Ren Yu Department of Pediatrics Chang Gung Memorial Hospital-Kaohsiung Medical Center Graduate Institute of Clinical Medical Science Chang Gung University College of Medicine Department of Pathology Chang Gung Memorial Hospital-Kaohsiung Medical Center Graduate Institute of Clinical Medical Science Chang Gung University College of Medicine

prenatal glucocorticoids （GCs） have been used to induce maturation of preterm fetal lungs and prevent the development of respiratory distress syndrome of the premature. Pulmonary surfactant induction has been regarded as the most important effect of prenatal GCs. However, report about the prolonged effects of prenatal GCs on the development of rat lung is of limited. In this study, we tried to investigate the acute and chronic modulation effects of prenatal dexamethasone （DEX） to asymmetric dimethylarginine （ADMA）/nitric oxide （NO） signal pathway of lung tissue. Pregnant Sprague Dawley rats at gestational day 14-20 were administered i.p. DEX （0.1 mg· kg-1 ·d-1）. Acute programming effects of prenatal DEX were assessed at postnatal day 7, and long-term programming effects of offspring were assessed at day 120. We found that repetitive prenatal DEX exposure contributes to DNA oxidative damage and alveolar tissue dysplasia. prenatal DEX treatment decreased ADMA and increased iNOS expres- sion. prenatal DEX treatment also increased TNF-α transcript expression and decreased HDAC2 protein expression at acute stage. In conclusion, repetitive prenatal DEX has prolonged stress damage effects on lung tissue.

关键词： prenatal glucocorticoids ADMA DNA oxidative damage TNF-α HDAC2 Lung dysplasia

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：