期刊文献+

大鼠局灶性脑缺血再灌注损伤神经细胞凋亡及尼莫地平干预的研究 被引量:1

The Effect of Nimodipine on The Neuron Apoptosis Following Focal Cerebral Ischemia-reperfusion on Middle Cerebral Artery in Rats
下载PDF
导出
摘要 目的:研究大鼠局灶性脑缺血再灌注后神经细胞凋亡的情况及尼莫地平干预的影响。方法:雄性Wistar大鼠120只,随机分为正常对照组、假手术组、脑缺血组和尼莫地平组,后两组按时间分成再灌注1、3、6、12、24,36、48、72h和7d组。制作MACO动物模型致大鼠形成局灶性脑缺血,记录大鼠的神经功能缺损情况,应用TUNEL法检测脑缺血再灌注后神经细胞凋亡的情况。结果:大鼠脑缺血再灌注损伤神经细胞凋亡缺血组各时间点同正常对照组、假手术组相比均明显增高,差异有统计学意义(P<0.05);尼莫地平干预后可以显著减少大鼠脑缺血再灌注损伤凋亡细胞数量(P<0.05)。结论:尼莫地平可以减少脑缺血再灌注后神经细胞凋亡,从而保护大鼠脑缺血再灌注脑细胞的损害。 Objective:To investigate the neuron apoptosis in the MCAO rat models of focal cerebral ischemia-reperfusion and the effect of nimodipine on them.Methods: 120 male Wistar rate weighing 250~300 g were randomly divided into four groups,normal group,sham operation group,cerebral ischemic group and nimodipine-applied group.Cerebral ischemic and nimodipine-applied groups were further divided into 1、3、6、12、24、36、48、72 hour and 7 days groups according to the time of reperfusion after cerebral ischemia respectively. Focal cerebral ischemic rat models were subjected to right middle cerebral artery occlusion(RMCAO)by a suture lasting for 2 hours and followed by reperfusion. Then record the neurologic impairment of these rats. Apoptosis was analyzed by TdT mediated dUTP - biotin nick end labeling using light microscope and image analysis system. Results: The number of apoptosis positive ceils in cerebral ischemic group at different time point were higher compared with sham operation and normal groups (P 〈 0.05). The number of apoptosim positive cells were decreased after using nimodipine(P 〈 0.05). Conclusion: Nimedipine might inhibit the development of neuron apoptosis in rats after ischemia and reperfusion and have the neuroprotective effect against ischemia and reperfusion injury.
出处 《内蒙古医学杂志》 2009年第7期769-772,共4页 Inner Mongolia Medical Journal
基金 包头市医药卫生基金项目(2006G2009-22)
关键词 大鼠 脑缺血再灌注 神经细胞凋亡 尼莫地平 Rats Cerebral ischemia-reperfusion Neuron apoptosis Nimodipine
  • 相关文献

参考文献5

二级参考文献15

  • 1刘斌,张宇,臧贺川,李世英,刘昊,张晋霞,伊红丽,石秋艳.藻酸双酯钠对大鼠脑缺血再灌注后神经细胞保护作用的研究[J].临床神经病学杂志,2005,18(5):363-366. 被引量:8
  • 2[1]Philip EB, Bonnie MH. Causes of calcium accumulation in rat cortical brain slice during hypoxia and ischemia: rile of ionchannels and mambrane damage.Brain Res, 1994,665: 269.
  • 3[2]Geoffrey CT, Robert MS. Mechanistic distinctions between exitotoxic and acidotic hippocampal damage in an in vitro model of ischemia. J Cereb Blood Flow Metab, 1990,10:527.
  • 4[3]Mitani A, Takeyasu S, Yanase H, et al. Changes in intracellular Ca2 + and energy levels during in vitro is-chemia in the gerbilhippocampal slice. J Neurochem,1994,62: 626.
  • 5[4]Kristian T, Gido G, Kuroda S, et al. Calcium metabolism of focal and penumbral tissues in rats subjected to transient middle cerebral artery occlusion. Exp Brain Res, 1998,120:503.
  • 6[5]Giffard RG, Monyer H, Christine CW, et al. Acidosis reduces NMDA receptor activation, glutamate neurotoxicity and oxygenglucose deprivation neuronal injury in cortical cuture. Brain Res, 1990,506: 339.
  • 7[6]Ebine Y, Fujiwara N, Shimoji K, et al. Mild acidosis inhibits the rise in intracellular Ca2 + concentration in response to oxygenglucose deprivation in mouse hippocampal slice. Neurosci Lett, 1994,168:155.
  • 8[7]Morishita E, Masuda S, Nagao M, et al. Erythropoietin receptor is expressed in rat hippocampal and cerebral cortical neurons, and Erythropoietin prevents in vitro glutamate-induced neuronal death. Neuroscience, 1997,76:105.
  • 9[8]Kristian T, Siesjo BK. Calcium in ischemic cell death. Stroke, 1998,29:705.
  • 10[9]Honda T, Fujiware N,Abe T, et al. Prior mechanical injury inhibits rise in intracellular Ca2+ concentration by oxygen-glucose deprivation in mouse hippocampal slice. Brain Res, 1994,666: 263.

共引文献22

同被引文献12

引证文献1

二级引证文献1

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