论文部分内容阅读
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-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)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-κB)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l L-1β、TNF-α以及IL-6的表达,明显减轻肺水肿,抑制NF-κB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。
AIM: To investigate the protective effect of N-myc downstream regulatory gene-2 (NDRG2) overexpression on lung ischemia-reperfusion injury in rats. Methods: The model of lung ischemia-reperfusion injury was established. NDRG2 was overexpressed in rat alveolar epithelial cells by tracheal instillation of the transfected NDRG2 recombinant adenovirus. Western blot was used to detect the expression of target protein in rat lung tissue. The levels of interleukin-1β, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and lung tissue wet / dry weight ratio (W / D) Detection of edema in lung tissue, dual luciferase reporter system to detect nuclear transcription factor kappa B (NF-κB) activity, HE staining to detect pathological changes in lung tissue. Results: Overexpression of NDRG2 could inhibit the expression of IL-1β, TNF-α and IL-6 in pulmonary ischemia-reperfusion injury and significantly reduce the pulmonary edema, inhibit the activity of NF-κB and the inflammation of pathological tissues change. Conclusion: Overexpression of NDRG2 can attenuate acute lung injury induced by ischemia-reperfusion, which may be related to its inhibition of inflammatory reaction.