| 陈家宽 王荣 李建忠 李晓平 张鸿 王文辰 夏彦民 周琳 葛忠虎 杨波 姜涛.N-myc 下游调节基因-2 过表达对大鼠肺缺血再灌注损伤的影响[J].,2016,16(15):2816-2819 |
| N-myc 下游调节基因-2 过表达对大鼠肺缺血再灌注损伤的影响 |
| Over-expression of N-myc DownstreamRegulated Gene 2 Improves LungIschemia-reperfusion Injury in Rats |
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| DOI： |
| 中文关键词: 肺缺血再灌注损伤 N-myc 下游调节基因-2 核转录因子kappa B 炎症因子 |
| 英文关键词: Lung ischemia-reperfusion injury N-myc downstreamregulated gene 2 Nuclear factor- kappa B Inflammatory factors |
| 基金项目:国家自然科学基金项目（81070062）；天津市卫生局面上项目（2013KY09） |
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| 中文摘要: |
| 摘要目的：研究N-myc 下游调节基因-2（NDRG2）过表达对大鼠肺缺血再灌注损伤的保护作用。方法：以肺缺血再灌注损伤为模
型，将已转染的过表达NDRG2 重组腺病毒经气管滴注的方法使大鼠肺泡上皮细胞NDRG2 过表达。用Western-blot 法检测大鼠
肺组织内目的蛋白过表达情况。用ELISA 法检测白细胞介素-1beta（IL-1beta）、肿瘤坏死因子-alpha（TNF-alpha）以及白细胞介素-6（IL-6）的
水平，肺组织湿干重比值（W/D）检测肺组织的水肿，双荧光素酶报告系统检测核转录因子kappa B（NF-kB）的活性，HE 染色检测肺组织病理变化。结果：在肺缺血再灌注损伤中，过表达NDRG2 可抑制炎症因子lL-1beta、TNF-alpha以及IL-6 的表达，明显减轻肺水
肿，抑制NF-kB 的活性和病理组织的炎性改变。结论：NDRG2 过表达可减轻缺血再灌注所致急性肺损伤，这可能与其抑制炎症反应有关。 |
| 英文摘要: |
| Objective:To investigate the protective effect of NDRG2 over-expression on the lung ischemia-reperfusion injury
(LIRI) in rats.Methods:The acute alveolar epithelial cell injury model was established by stimulation with LIRI. In order to over-express
NDRG2, the lung tissues were transferred with recombinant adenovirus via tracheal instillation method. The concentrations of IL-1beta,
TNF-alphaand IL-6 were detected by ELISA. Pulmonary edema was measured by wet-to-dry weight ratio. The transcriptional activity of
NF-kB was measured by dual-luciferase reporter assay system. The effects of NDRG2 on lung ischemia-reperfusion induced lung pathological
changes were examined.Results:Compared with the control group, NDRG2 over-expression could decrease the releases of IL-1beta,
TNF-alpha and IL-6 stimulated by LIRI. The lung wet-to-dry weight ratio was markedly decreased by NDRG2 over-expression. The over-expression
NDRG2 inhibited the transcriptional activity of NF-kB and the pathological changes in the lung.Conclusion:NDRG2 over expression
could attenuate the inflammatory reactions in LIRI, which played a protective role against the acute damage of the alveolar epithelial
cells. |
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