期刊文献+

去铁胺和缺氧缺血性脑损伤 被引量:2

Deferoxamine and hypoxic ischemic brain damage
原文传递
导出
摘要 去铁胺是一种铁离子螯合剂,具有神经保护作用,能通过螯合铁离子阻断羟自由基的形成,减轻脂质过氧化损伤,减少细胞凋亡。近年研究表明,去铁胺主要通过稳定缺氧诱导因子1α的表达及诱导其靶基因的转录对缺氧缺血性脑损伤后细胞的修复起到积极作用;此外去铁胺还能阻止中性粒细胞介导的细胞损伤。目前去铁胺对缺氧缺血性脑损伤的治疗研究尚处于动物实验阶段,在损伤前或损伤后给予去铁胺均能对脑组织起到保护作用,为临床应用去铁胺提供了实验依据。现对去铁胺的作用机制及应用进展予以综述。
出处 《国际儿科学杂志》 2008年第2期103-105,共3页 International Journal of Pediatrics
基金 国家自然科学基金资助项目(30570623) 四川大学华西医学中心CMB项目资助(00-722) 教育部留学回国人员启动基金资助项目(2006331-11-7)
  • 相关文献

参考文献17

  • 1Sorond FA, Ratan RR. Ironing-out mechanisms of neuronal injury under hypoxie-ischemic conditions and potential role of iron chelators as neuroprotective agents. Antioxid Redox Signal, 2000,2 (3) : 421-436.
  • 2Selim MH, Ratan RR. The role of iron neurotoxicity in ischemic stroke. Ageing Res Rev,2004,3(3):345-353.
  • 3Rogalska J, Danielisova V, Caputa M. Effect of neonatal body temperature on postanoxic, potentially neurotoxic iron accumulation in the rat brain. Neurosci Lett, 2006, 393 (2-3) : 249-254.
  • 4Sugawara T, Fujimura M, Ncshita N, et al. Neuronal death/survival signaling pathways in cerebral ischemia. NeuroRx, 2004,1 ( 1 ) : 17-25.
  • 5Bishop GM, Robinson SR. Quantitative analysis of cell death and ferritin expression in response to cortical iron: implications for hypoxia-ischemia and stroke. Brain Res,2001,907(1-2) : 175-187.
  • 6Palmer C, Menzies SL, Roberts RL, et al. Changes in iron histochemistry after hypoxic-ischemic brain injury in the neonatal rat. J Neurosci Res, 1999,56(1) :60-71.
  • 7黄越芳,庄思齐,梁英杰,陈东平,李晓瑜.去铁胺对新生大鼠缺氧缺血性脑损伤的保护作用[J].广东医学,2003,24(7):695-697. 被引量:3
  • 8Mu D, Chang YS, Vexler ZS, et al. Hypoxia-inducible factor lalpha and erythropoietin upregulation with defemxamine salvage after neonatal stroke. Exp Neurol,2005,195(2) :407-415.
  • 9Hamrick SE, McQuillen PS, Jiang X, et al. A role for hypoxia-inducible factor-lalpha in desferoxamine neuroprotection. Neurosci Lett, 2005, 379 (2) :96-100.
  • 10Zaman K, Ryu H, Hall D, et al. Protection from oxidative stress-induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia-inducible factor-1 and ATF-1/CREB and increased expression of glycolytic enzymes, p2^lwaf1/cip1, and erythropoietin. J Neurosci, 1999,19(22) :9821-9830.

二级参考文献9

  • 1Rice JE. Vannucci RC, Briedey JB. The influence of immaturity on hypoxic- ischemic brain damage in the rat. Ann Neurol, 1981,9(2) : 131.
  • 2Nelson CW, Wei EP, Povlishock IF, et al. Oxygen radicals in cerebral ischemia. ,Mn J Physiol, 1992,263(5Pt 2) : H1356.
  • 3Halliwell B. Gutteridge JM. Oxygen toxicity, oxygen radicals, transition metals and disease. Biochem J, 1984,219( 1 ) : 1.
  • 4Yonezawa M, Back SA, Gan X. Cystine deprivation induces oligodendroglial death: rescue by free radical scavengers and by a diffusible glial factor. J Neurochem, 1996,67 (2) : 566.
  • 5Kompala SD, Babbs CF, Blaho KE. Effect of deferoxamine on late deaths following CPR in rats. Ann Emerg Med, 1986, 15(4) :405.
  • 6Jones NM, Bergeron M. Hypoxic preconditioning induces changes in HIF- 1 target genes in neonatal rat brain. J Cereb Blood Flow Metab,2001,21(9):1105.
  • 7Wang GL, Semenza GL. Desferrioxamine induces erythropoietin gene expression and hypoxia- inducible factor 1 DNA - binding activity: implications for models of hypoxia signal transduction. Blood, 1993, 82(12) :3610.
  • 8Zaman K. Protection from oxidative stress - induced apoptosis in cortical neuronal cultures by iron chelators is associated with enhanced DNA binding of hypoxia - inducible factor- 1 and ATF - 1/CREB and increased expression of glycolytic enzymes, p21 (waf1/cip1), and erythropoletin. J Neurosci, 1999,19(22) :9821.
  • 9Harik SI, Behmand RA, LaManna JC. Hypoxia increases glucose transport at blood - brain barrier in rats. J Appl Physiol, 1994, 77(2) : 896.

共引文献2

同被引文献31

  • 1Kontos I-IA, Povlishock JT. Oxygen radi- cals in brain injury [J]. Cent Nerv Syst Trauma, 1986, 3(4): 257-263.
  • 2Zaleska MM, Floyd RA. Regional lipid peroxidation in rat brain in vitro: possible role of endogenous iron [J]. Neurochem Res, 1985, 10(3): 397-410.
  • 3Sadrzadeh SM, Eaton JW. Hemoglobin- mediated oxidant damage to the central nervous system requires endogenous ascorbate [J]. Clin Invest, 1988, 82 (5): 1530-1515.
  • 4Radi R. Peroxynitrite reactions and diffu- sion in biology [J]. Chem. Res. Toxicol, 1998, 11(7): 720-721.
  • 5Gahm C, Holmin S, Mathiesen T. Tempo- ral profiles and cellular sources of three nitric oxide synthase isoforms in the brain after experimental contusion [J]. Neuro- surgery, 2000, 46(1): 169-177.
  • 6Mosenge C, Margaill I, Verreechia C, et al. Protective effect of melatonin in a model of traumatic brain injury in mice[J]. Pineal Res, 1998, 25(1): 41-46.
  • 7Reed TT, Owen J, Pierce WM, et al. Pro- teomic identification of nitrated brain pro- teins in traumatic brain-injured rats treated postinjury with gamma-glutamyl- cysteine ethylester: insights into the role of elevation of glutathione as a potential therapeutic strategy for traumatic brain injury [J]. J Neurosci Res, 2009, 87 (2): 408- 417.
  • 8Mikawa S, Kinouchi H, Kamii H, etal. Attenuation of acute and chronic damage following traumatic brain injury in copper, zinc -superoxide dismutase transgeuic mice [J]. Neurosurg, 1996, 85 (5): 885- 891.
  • 9Muizelaar JP, Marmarou A, YoungHF, etal. Improving the outcome of" severe head injury with the oxygen radical scavenger polyethylene glycol-conjugated superoxide dismutase: a phase II trial [J]. Neurosurg. 1993, 78(3): 375-382.
  • 10Muizelaar JP, Kupiee JW, Rapp LA. PEG- SOD after head injury [J]. Neurosurg, 1995, 83(5): 942.

引证文献2

二级引证文献10

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