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高压氧治疗外伤性癫痫大鼠模型的机制 被引量:5

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摘要 目的探讨高压氧治疗外伤性癫痫的机制。方法采用大脑皮层注射氯化亚铁建立外伤性癫痫大鼠模型,将癫痫大鼠分为无接受高压氧治疗的模型组及接受高压氧治疗的治疗组,将正常大鼠设立为正常组,对3组进行行为学观察及脑电图记录。取脑组织观察神经细胞形态改变,检测各组标本c-fos m RNA、c-jun m RNA、c-myc m RNA的表达水平。结果治疗组脑细胞形态学改变相对于模型组更少有神经元变性及凋亡。治疗组的c-jun m RNA、c-myc m RNA的表达水平较模型组明显下降(P<0.01)。结论高压氧治疗外伤性癫痫通过阻断c-jun、c-myc基因介导的细胞凋亡通路而起到治疗效果。
出处 《广东医学》 CAS 北大核心 2015年第1期60-62,共3页 Guangdong Medical Journal
基金 广东省科技计划项目(编号:2011B031800109)
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参考文献12

  • 1FERGUSON P L,SMITH G M, WANNAMAKER B B, et al. Apopulation - based study of risk of epilepsy after hospitalization fortraumatic brain injury[ J] . Epilepsia, 2010,51(5) : 891 -898.
  • 2ZHAO Y,WU H,WANG X, et al. Clinical epidemiology of post-traumatic epilepsy in a group of Chinese patients [ J ]. Seizure,2012,21(5) : 322 -326.
  • 3YANG K, MU X S,XUE J J, et al. Increased expression of c -fos raRNA and AP -1 transcription factors after cortical impact in-jury in rats[ J]. Brain Res, 1994, 664(1/2) ; 141 - 147.
  • 4WEY A, KNOEPFLER P S. c - myc and N - myc promote activestem cell metabolism and cycling as architects of the developingbrain[ J]. Oncotarget, 2010,1(2): 120 -130.
  • 5林元相广州,徐如祥,姜晓丹,康德智,柯以铨,周谷兰,杜谋选,蔡颖谦,秦玲莎.皮层注射氯化亚铁建立外伤性癫痫动物模型[J].中华神经医学杂志,2006,5(4):372-377. 被引量:34
  • 6SPIGOLON G, VERONESI C, BONNY C, et al. c-Jun N - ter-minal kinase signaling pathway in excitotoxic cell death followingkainic acid - induced status epilepticus [ J ]. Eur J Neurosci,2010,31(7) ; 1261 -1272.
  • 7GAO Y, SIGNORE A P, YIN W, et al. Neuroprotection againstfocal ischemic brain injury by inhibition of c - Jun N - terminal ki-nase and attenuation of the mitochondrial apoptosis - signalingpathway[ J] . J Cereb Blood Flow Metab, 2005,25(6) : 694 -712.
  • 8JOHNSON G L,NAKAMURA K. The c - jun kinase/ stress - acti-vated pathway : regulation, function and role in human disease[J] . Biochim Biophys Acta, 2007 , 1773 ( 8) : 1341 — 1348.
  • 9姜曙,于如同,毛伯镛,高立达.脑损伤诱导神经细胞凋亡的动物实验研究[J].华西医科大学学报,2000,31(3):358-361. 被引量:17
  • 10STOICA B A, FADEN A I. Cell death mechanisms and modula-tion in traumatic brain injury [ J ]. Neurotherapeutics, 2010, 7.1): 3-12.

二级参考文献19

  • 11.Dixon CE, Lyeth BG, Povlishock JT, et al. A fluid percussion model of experimental brain injury in the rat. J Neurosurg, 1987; 67(1):110
  • 22.Tominaga T, Kure S, Narisawa K, et al. Evidence of apoptosis cell death after focal cerebral ischemia. Brain Res;1993; 624(1):32
  • 33.Rink A, Fungkar M, Trojanowski JQ, et al. Evidence of apoptosis cell death after experience traumatic brain injury in the rat. Am J Pathol, 1995; 147(6):1575
  • 44.Rothstein JD, Bristol LA, Hosler, et al. Chronic inhibition of superoxide dismutase produces apoptotic death of spinal neurons. Proc Natl Acd Sci USA, 1994; 91:4155
  • 55.Clark RS, Cheng J, Watkins SC, et al. Apoptosis-supressor gene Bcl-2 expression after traumatic brain injury in rats. J Neurosci, 1997; 17:9172
  • 66.Rchristain C, Amy LT, Philip F. Morgan attenuation of P53 expression protects against focal ischemia damage in transgenic mice. J Cere Blood Flow Met, 1994; 14:887
  • 77.Grove M, Plumb M. NF-KB and C-Ets family members and transcriptional regulation of the cell-specific and inducible macrophage inflammatory protein-1 in mediated-early gene. Mol Cell Biol, 1993; 13(9):5276
  • 88.Masato T, Hinoshi L, Susumu A, et al. Hypoxia induces apoptosis with enhanced expression of Fas antigen message RNA in cultured rat cardiomyocytes. Circulation Research, 1994; 75(3):426
  • 99.Colicos Ma, Dixon CE, Dash PK. Delayed selective neuronal death following experimental impact injury in rats: possible role in memory deficits. Brain Res, 1996; 739(13): 111
  • 1010.Sinson G. Improvement of cognitive deficits and decreased cholinergic cell loss and apoptotic cell death following neurotrophin infusion after experimental traumatic brain injury. J Neurosury, 1997; 86(3):511

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