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选择性亚低温对脑外伤大鼠脑组织Fas-L基因表达的影响

Effects of Selective Mild Hypothermia on Expression of Fas ligand mRNA in Rats After Traumatic Brain Injury
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摘要 目的研究选择性亚低温治疗大鼠脑外伤时对脑组织Fas-L基因表达的影响。方法 72只大鼠随机分为假手术组、亚低温组和常温对照组。采用改进的Feeney自由落体法制作重型外伤性颅脑损伤模型,局部降温法在伤后30min内达到亚低温目标并保持6h,RT-PCR检测3组大鼠伤后不同时间点脑组织Fas-L基因表达。结果亚低温组大鼠在损伤后不同时间点(6h,24h,48h和72h)脑组织的Fas-LmRNA的相对含量分别为0.54±0.07、0.47±0.06、0.41±0.06、0.67±0.08,常温对照组分别为1.53±0.21、0.91±0.11、1.33±0.15、1.56±0.171.53,相同时间点两组间比较均有显著性差异(P<0.05)。结论亚低温对大鼠外伤性颅脑损伤急性期具有降低Fas-LmRNA的作用。 Objective To study the effects of local mild hypothermia on Fas ligand (Fas-L) mRNA in rats after traumatic brain injury. Methods Seventy-two Sprague-Dawley rats were randomly divided into sham-operation group, mild hypothermia group and normothermia group. Feeney' s model was used to produce traumatic brain injury. Local therapeutic hypothermia was achieved 30 minutes after injury by surface cooling and maintained for 6 hours. The expression of brain Fas- L mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Results The expression of rat brain Fas-L mRNA in the mild hypothermia group was much lower than that in the normothermia group at 6 hours, 24 hours after injury ( 0.54, 0.47, 0.41 and 0.67 versus 1. 53, 0. 917, 1. 33 and 1. 56, respectively, P 〈0.05). Conclusion Mild hypothermia can down-regulate the Fas-L expression of brain tissue in the acute phase of traumatic brain injury.
出处 《健康研究》 CAS 2010年第2期92-94,共3页 Health Research
基金 杭州市医药卫生科技计划项目(2007A011)
关键词 选择性亚低温 脑损伤 脑水肿 Fas—L基因 大鼠 Selective mild hypothermia brain injury, traumatic Fas ligand RT- PCR rats
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  • 1王光伟,刘运生,梁有明,屈洪涛,李创华.重型颅脑外伤局灶低温疗法的实验研究[J].医学临床研究,2004,21(6):616-619. 被引量:4
  • 2裘五四,王毓璈,余国良.亚低温对小鼠局灶性脑缺血的保护作用[J].杭州医学高等专科学校学报,2004,25(6):274-276. 被引量:4
  • 3[1]Martin VA, Herr I, Jeremias I, et al. CD95 ligand(FasL/APO 1L) and tumor necrosis factor related apoptosis inducing ligand mediate i schemia induced apoptosis in neuron[J]. J Neurosci,1999,19(10):3809-3817.
  • 4[2]Feeney DM, Boyeson MG, Linn RT, et al. Responses to cortical inj ury:Ⅰ.Methodology and local effects of contusions in the rat[J]. Brain Res,1 981,211(1):67-77.
  • 5[3]Clifton GL, Jiang JY, Lyeth BG,et al. Marked protection by moder ate hypothermia after experimental traumatic brain injury[J]. J Cereb Blood Fl ow Metab,1991,11(1):114-121.
  • 6[4]Ertel W, Keel M, Stocker R, et al. Detectable concentrations of Fas ligand in cerebrospinal fluid after severe head injury[J]. J Neuroimmunol ,1997,80(1-2):93-96.
  • 7[5]Gass P, Spranger M, Herdegen T, et al. Induction of Fos and Jun proteins after focal ischemia in the rat:differential effect of the N methyl- D-asparate receptor antagonist MK-801[J]. Acta Neuropathol,1992,84(5):545- 553.
  • 8[6]Beer R, Franz G, Schopf M, et al. Expression of Fas and Fas liga nd after experimental traumatic brain injury in the rat[J]. J Cereb Blood Flow Metab,2000,20(4):669-677.
  • 9[7]Yakovlev AG, Knoblach SM, Fan L, et al. Activation of CPP32-lik e proteases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury[J]. J Neurosci,1997,17(19):7415-7424.
  • 10[8]Shin SW, Park JW, Suh MH, et al. Persistent expression of Fas/F asL mRNA in the mouse hippocampus after a single NMDA injection[J]. J Neuroche m,1998,71(4):1773-1776.

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