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异丙酚对原代培养海马神经元缺氧反应的影响 被引量:14

Effects of propofol on the anoxic response of primary cultured hippocampal neurons
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摘要 目的 观察不同浓度异丙酚对原代培养海马神经元缺氧反应的影响。方法 培养 12d海马神经元 ,随机分为四组 :正常对照组、缺氧组、缺氧加异丙酚 5 0 μmol L组 ,缺氧加异丙酚 5 0 0 μmol L组。测定乳酸脱氢酶 (LDH)漏出率及c fos免疫组化。结果 位于细胞核内的c fos阳性蛋白缺氧前染色为浅紫色 ,缺氧后呈紫黑色且阳性细胞数量增加 (P <0 0 1) ,而加入异丙酚后能减少这种反应。缺氧组LDH漏出率较正常组增加 (P <0 0 1) ,异丙酚组能降低缺氧组增加的LDH漏出率 (P <0 0 5 ) ,且与异丙酚剂量有关。结论 异丙酚能提高体外海马神经元的缺氧耐力 ,减少LDH漏出率和c fos蛋白过度表达。 Objective To evaluate the effects of different concentration of propofol on the anoxic response of primary cultured hippocampal neurons Methods Newborn (<24h) Wistar rats were used Hippocampal neurons having been cultured for 12 d were randomly divided into four groups: control group, anoxia group, propofol 50μmol/L group , anoxia+propofol 500μmol/L group Lactic dehydrogenase(LDH) efflux ratio was assayed and c fos protein immunohistochemical staining were performed in every group Results The c fos protein expression in propofol groups was significantly less than that in anoxia group LDH efflux ratio significantly increased in anoxia groups(P<0 01) as compared with that in control group Propofol reduced the increase in LDH efflux induced by anoxia in a concentration dependent manner Conclusions Propofol can enhance the tolerance of anoxia in primary cultured hippocampal neurons by decreasing LDH efflux ratio and c fos protein expression
出处 《中华麻醉学杂志》 CAS CSCD 北大核心 2001年第8期473-475,共3页 Chinese Journal of Anesthesiology
基金 1999年北京卫生重点扶植学科联合资助项目 (0 6)
关键词 二异丙酚 低氧 海马 神经元 FOS基因 乳酸脱氢酶 麻醉药 Propofol Anoxia Hippocampus Neurons Genes,fos Lactate dehydrogenase
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  • 1王福庄,J Neurosci Res,1990年,25卷,312页
  • 2王福庄,J Physiol Sci,1989年,5卷,4期,277页
  • 3丁爱石,军事医学科学院院刊,1988年,12卷,5期,377页
  • 4王祥瑞,当代麻醉与复苏,1994年,26页
  • 5季健平,南京铁道医学院学报,1991年,10卷,27页

共引文献105

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  • 1王晓薇,邵建林,黄海琼,黄青青.异氟醚诱导大鼠中枢神经系统c-fos基因的表达[J].昆明医学院学报,2004,25(3):4-8. 被引量:5
  • 2陈君,王国林.异丙酚预先给药对缺氧复氧鼠脑神经元的保护作用[J].中华麻醉学杂志,2004,24(8):591-595. 被引量:3
  • 3赖虹,吕永利.海马与衰老[J].解剖科学进展,1995,1(1):91-96. 被引量:10
  • 4顾健腾,陶国才.蛋白质芯片与全身麻醉机制[J].国外医学(麻醉学与复苏分册),2005,26(4):203-205. 被引量:1
  • 5[3]Sagara Y, Hendler S, Sue KR, et al. Propofol hemisuccinate protects neuronal cells from oxidative injury. J Neurochem, 1999,73: 2524 ~2530.
  • 6[4]Cervantes M, Ruelas R, Carrillo CI, et al. Effects of propofol on alterations of multi-neuronal activity of lim-ibic anc mesencephalic cerebral ischemia. Arch Med Res, 1995,26:385 ~ 395.
  • 7[7]Yavin E, Billia DM. Apoptotic death in cerebral hemisphere cells is dependent and modulated by transient oxygen and glucose deprivation. J Neurosci Res, 1997,47:471 ~ 478.
  • 8[8]Nagata A, Nakao S, Estuko M, et al. Propofol inhibits ketamine in-duced C-fos expression in the rat posterior cingulate cortex. Anesth Analg, 1998,87:1416 ~ 1420.
  • 9[9]Nakki R,Sharp FR,Sagar SM ,et al. Effects of phencyclidine on immediate early gene expression in the brain. J Neurosci Res, 1996,45:13 ~27.
  • 10[9]Hermann D M,Kilic E,Hata R,et al.Relationship between metabolic dysfunctions,gene responses and delayed cell death after mild focal cerebral ischemia in mice[J].Neuro-science,2001,104 (4):947-949.

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