期刊文献+

依达拉奉对高氧损伤小鼠肺组织中白介素-4、干扰素-γ、转化生长因子-β_1的影响

Impact of Edaravone on hyperoxic lung injury in neonatal mice
在线阅读 下载PDF
导出
摘要 目的探讨依达拉奉对新生小鼠高氧肺损伤的治疗作用,为临床防治新生儿高氧肺损伤提供理论依据。方法将新生小鼠随机分为空气+生理盐水组、空气+依达拉奉组、高氧+生理盐水组、高氧+依达拉奉组,于实验第3、7、10、14和21天取材,测定肺组织中白介素-4(IL-4)、干扰素-γ(IFN-γ)、肺组织中转化生长因子-β_1(TGF-β_1)表达的变化。结果随着吸氧时间的延长,高氧组IL-4、IFN-γ含量均高于空气组且比例失衡,TGF-β_1表达越多并肺组织结构紊乱;依达拉奉治疗组IFN-γ含量显著增高,IL-4含量明显降低,IFN-γ/IL-4比值更接近正常组,TGF-β_1表达降低,肺组织结构较高氧组好转。结论高氧可导致新生小鼠急性肺损伤;依达拉奉可调节IFN-γ、IL-4的含量及比例,降低TGF-β_1的表达,发挥对高氧肺损伤的防治作用。 Objective To explore the effects of Edaravone in hyperoxic lung injury in neonatal mice so as to provide experimental and theoretical evidences for controlling hyperoxic lung injury in neonate. Methods Neonatal mice were randomly divided into air + normal saline, air + Edaravone, hyperoxia + normal saline,hyperoxia + Edaravone groups. At the end of exposure(on the 3rd, 7th, 10 th, 14 th and 21 st day), IL-4 and IFN-γ in lung homogenate were evaluated by ELISA, and TGF-β1and optical density(OD) in lung slices were determined using immunohistochemical stain and computerized graphic analysis techniques. Results With the increasing time of exposure, IL-4, IFN-γ and TGF-β1of the hyperoxic group were increasing and higher than those in the air group, lung injury also aggravated. Compared to the hyperoxic group, the treatment group showed increased IFN-γ and decreased IL-4 and TGF-β1; histopathological changes were alleviated as well. Conclusions Hyperoxia can result in acute lung injury in neonatal mice. Edaravone can regulate the content and ratio of IFN-γ and IL-4, decrease the expression of TGF-β1, thus play a role in prevention and treatment of hyperoxic lung injury.
出处 《中国现代医学杂志》 CAS 北大核心 2016年第9期29-33,共5页 China Journal of Modern Medicine
关键词 依达拉奉 肺损伤 高氧 白介素-4 干扰素-Γ 转化生长因子-β_1 新生小鼠 Edaravone lung injury hyperoxia IL-4 IFN-γ TGF-β1 neonatal mouse
  • 相关文献

参考文献21

  • 1马丽亚,常立文,全裕凤.L-NAME对新生大鼠高氧肺损伤的影响[J].同济医科大学学报,2000,29(2):157-159. 被引量:9
  • 2DUTKA T L, VERBURG E, LARKINS N, et al. ROS-mediated decline in maximum Ca2+-activated force in rat skeletal muscle fibers following in vitro and in vivo stimulation[J]. PLoS One, 2012, 7(5): e35226.DOI: 10.1371/journal.pone.0035226.
  • 3SCHOELER M, LOETSCHER P D, ROSSAINT R, et al. Dexmedetomidine is neuroprotective in an in vitro model for traumatic brain injury[J]. Bmc Neurology, 2012, 12(1): 1-7.
  • 4KIKUCHI K, KAWAHARA KI, UCHIKADO H, et al. Potential of edaravone for neuroprotection in neurologic diseases that do not involve cerebral infarction (Review)[J]. Experimental Therapeutic Medicine, 2011, 2(5): 771-775.
  • 5李平,汪波.依达拉奉联合溶栓治疗急性脑梗死的疗效及对氧自由基清除效果的影响[J].中国现代医学杂志,2015,25(28):49-52. 被引量:59
  • 6YANG T, ZHANG J, SUN L, et al. Combined effects of a neutrophil elastase inhibitor (sivelestat sodium) and a free radical scavenger (edaravone) on lipopolysaccharide-induced acute lung injury in rats[J]. Agents Actions, 2012, 61(6): 563-569.
  • 7施梦,王宜青,庞烈文,黄杰春,曹同瓦,白春学.依达拉奉对大鼠急性肺损伤的干预作用[J].中华胸心血管外科杂志,2009,25(6):402-405. 被引量:2
  • 8ZHANG G L, ZHANG W G, DU Y, et al. Edaravone ameliorates oxidative damage associated with Aβ25-35 treatment in PC12 cells[J]. Journal of Molecular Neuroscience, 2013, 50(3): 494-503.
  • 9UCHIYAMA M, TOJO K, YAZAWA T, et al. Edaravone prevents lung injury induced by hepatic ischemia-reperfusion[J]. Journal of Surgical Research, 2015, 194(2): 551-557.
  • 10WANG Z, LI R, LIU Y, et al. Protective effects of edaravone combined puerarin on inhalation lung injury induced by black gunpowder smog[J]. International Immunopharmacology, 2015, 26(1): 125-132.

二级参考文献27

  • 1Tanaka M. Pharmacological and clinical profile of the free radical scavenger edaravone as a neuroprotective agent. Nippon Yakurigaku Zasshi ,2002,119:301 - 308.
  • 2Hadjiminas DJ, McMasters KM, Peyton JC, et al. Tissue tumor necrosis factor mRNA expression following cecal ligation and puncture or intraperintoneal injection of endotoxin. J Surg Res, 1994,56:549 - 555.
  • 3Weinacker AB, Vaszar LT. Acute respiratory distress syndrome: physiology and new management strategies. Annu Rev Med,2001, 52:221 - 237.
  • 4Goldstein B, Giroir B, Randolph A, et al. International pediatric sepsis consensus conference : definitions for sepsis and organ dysfunction in pediatrics. Pediatr Cfit Care Med,2005,6..2 -8.
  • 5Marsh C B, Wewers MD. The pathogenesis of sepsis. Factors that modulate the response to gram-negative bacterial infection. Clin Chest Med, 1996,17 : 183 - 197.
  • 6Krawisz JE, Sharon P, Stenson WF. Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity. Assessment of inflammation in rat and hamster models. Gastroenterology, 1984, 87:1344 - 1350.
  • 7McCord JM. Oxygen-derived free radicals in postischemic tissue injury. New England Journal of Medicine, 1985,312 : 159 - 163.
  • 8Jurmann MJ, Dammenhayn L, Schaefers HJ, et al. Pulmonary reperfusion injury: evidence for oxygen-derived free radical mediated damage and effects of different free radical scavengers. Eur J Cardiothorac Surg, 1990,4:665 - 670.
  • 9All S, Mann DA. Signal transduction via the NF-KB pathway: a targeted treatment modality for infection, inflammation and repair. Cell Biochem Funct ,2004,22:67 - 79.
  • 10Hussain N, Wu E, Zhu L, et al. Neutrophil apoptosis during the development and resolution of oleic acid-induced acute lung injury in the rat. Am J Respir Cell Mol Biol,1998,19:867 -874.

共引文献67

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部