期刊文献+

弥漫性脑损伤中iNOSmRNA的表达及与脑水肿的相关性研究 被引量:1

Expression of iNOSmRNA and Relationship with Edema of Brain after Diffuse Injury
下载PDF
导出
摘要 目的探讨弥漫性脑损伤脑组织不同时间段iNOSmRNA表达及与脑组织水肿的关系。方法依据Marmarou's弥漫性脑损伤动物模型有改进,应用SD雄性大鼠55只,随机分为两组:假手术(对照组)(n=5)和弥漫性脑损伤组(n=50),损伤组再按照不同时间段分组(n=5),损伤后大鼠自由进食饮水,按0.5h、1h、3h、6h、12h、24h、48h、72h、1w、2w等时间段处死大鼠,提取大鼠皮层脑组织,一部分脑组织应用realtime RT-PCR检测对照组与不同时间段外伤组iNOSmRNA表达,另取一部分脑组织蘸干脑组织血迹,应用分析天平测定脑组织湿重,放入C101型电热恒温鼓风干燥箱105℃烘干至恒重,应用分析天平测定脑组织干重,应用脑组织干湿重比表示脑组织含水量。结果对照组,0.5h、1h、3h、6h、12h、24h、48h、72h、1w、2w时间段外伤组iNOSmRNACt值分别为:(34.999±0.444),(35.931±0.409),(40.376±0.551),(41.263±0.755),(42.539±0.394),(44.325±0.171),(44.165±0.255),(41.514±0.374),(41.390±0.158),(41.317±0.245),(35.204±0.504)。用kurskal-wallis秩和检验P<0.05,对照组不同时间组之间差别有统计学意义;脑组织含水量分别为:(0.78118±1.0532)E,(0.78505±1.6969)E,(0.79998±9.7477)E,(0.80231±3.4466)E,(0.80342±8.5095)E,(0.80913±1.0123)E,(0.80455±3.7740)E,(0.80196±5.5710)E,(0.80022±5.6378)E,(0.79998±5.2919)E,(0.78505±1.6969)E。用kurskal-wallis秩和检验P<0.01,对照组不同时间组之间含水量差别有统计学意义。结论①弥漫性脑损伤后脑组织iNOSmRNA表达早期有升高趋势,12h达到高峰,24h仍然处于高水平状态,随后下降,持续时间长达1周。②弥漫性脑损伤后脑组织含水量增加,6h增幅快,12h到达较高水平,持续两周。③iNOSmRNA表达可能是脑组织含水量增加的一个原因,且可能是脑组织含水量增高长期性的一个原因。 Objective To determine and evaluate the transformation of the edema and the expression of iNOSmRNA in brain following diffuse brain injury (DBI). Methods Fifty -five male SD rats were randomly divided into two groups: control ( n = 5 ), DBI (they were divided into ten groups again, n = 5). Diffuse contusion and laceration of brain was produced by Marmarou's brain injury model. Determine and evaluate the water contained in brain (edema of brain) and the expression of iNOSmRNA by realtime RT - PCR at different time following diffuse brain injury. Results The expression of iNOSmRNA upregulates rapidly following diffuse brain injury. The expression of iNOSmRNA gets to top at 12 hours. The expression of iNOSmRNA are different among groups by karskal - wallis test, P 〈 0.05. The water contained in damaged brain increase rapidly in 6 hours. The water contained in damaged brain are different among groups by kurskal - wallis test, P 〈 0.05. It gets to maximum at 12 hours. Conclusion (1) the expression of iNOSmRNA upregulates rapidly following diffuse brain injury. It gets to maximum at 12 hours. (2)The water contained in damaged brain increase rapidly at short time. It can reach higher leval at 6 hours. (3)the expression of iNOSmRNA following diffuse brain injury may be the cause that the water contained in damaged brain increase rapidly.
作者 李玉
出处 《医药论坛杂志》 2008年第14期1-3,8,共4页 Journal of Medical Forum
关键词 弥漫性脑损伤 一氧化氮合酶 脑水肿 Diffuse brain injury iNOS Brain edema
  • 引文网络
  • 相关文献

参考文献9

  • 1Moneada S,Palner R M, Higgs E A, Nitric oxide: physiology - pathophysiology, and pharmacology [ J ]. Pharmacol Rev, 1991,43 (2) : 109-142
  • 2Moncada S, Higgs EA. Molecular mechanisms and therapeutic strategics related to nitric oxide [ J ]. FASEB J, 1995,9:1 319-1 330
  • 3Vallance P, Collier J, Moncada S. Effects of endothelium -derived nitric oxide on peripheral arteriolar tone in man [J]. Lancet, 1989:2(8670) :997-1 000
  • 4Loscalzo J, Welch G. Nitric oxide and its role in the cardiovascular system [ J ]. Prog cardiovas Dis, 1995,38 (2) : 87-104
  • 5Dawson VL, Brahmbhatt HP, Mong JA, et al. Expression of inducible nitric oxide synthase causes delayed neurotoxicity in primary mixed neuronal- glial cortical ultures [ J]. Neuropharmacology, 1994,33 ( 11 ) : 1 425-1 430
  • 6Iadecola C, Zhang F, Xu XH. Inhibition of inducible nitric oxide synthase ameliorates cerebral ischemic damage [J]. Am J Physiol, 1995,268(1Rt2) :286-292
  • 7Dawson VL, Dawson TM, London ED, et al. Nitric oxide mediates glutamate neurotoxicity in primary cortical culture [J]. proc Natl Acad Sci USA, 1991,88:6 368-71
  • 8李光宇,赵彦艳,杨国瑞.大鼠弥漫性脑损伤后脑组织一氧化氮和一氧化氮合酶表达变化[J].中华创伤杂志,2006,22(6):462-463. 被引量:3
  • 9Hutterman M. Lee I,Kreipke CW, Petrov J. Suppression of the inducible form of nitric oxide synthase prior to traumatic brain injury improves sytochromec oxidaxe activity and normalizes cellular energy levels [ J ]. Neuroscience. 2008 Jan 2;151(1) :148-151

二级参考文献6

  • 1王成彬,沈文梅,田亚平,张道强,谭平,汪德清.铜离子活化镉还原法测定血清中硝酸盐浓度[J].中华医学检验杂志,1996,19(5):281-283. 被引量:47
  • 2Huang Z, Huang PL, Ma J, et al. Enlarged infarcts in endothelial nitric oxide synthase knockout mice are attenuated by nitro - L -arginine. J Cereb Blood Flow Metab, 1996,16:981 - 987.
  • 3Dawson VL, Kizushi VM, Huang PL, et al.Resistance to neurotoxicity in cortical cultures from neuronal nitric oxide synthase deficient mice. J Neurosci, 1996, 16:2479 -2487.
  • 4Mamarou A, Foda MA, van den Brink W, et al. A new model of diffuse brain injury in rats. Part Ⅰ. Pathophysiology and biomechanics. J Neurosurg, 1994, 80:191 -300.
  • 5Jones NC, Constantin D, Gibson CL, et al.A detrimental role for nitric oxide synthase -2 in the pathology resulting from acute cerebral injury. J Neuropathol Exp Neurol,2004, 63:708 - 720.
  • 6冯海龙,高立达,黄光富,谭海斌,廖晓灵,陈勇.大鼠重型脑伤后一氧化氮诱生型一氧化氮合酶神经细胞毒性的作用机制[J].中华创伤杂志,2000,16(7):416-418. 被引量:16

共引文献2

同被引文献8

引证文献1

二级引证文献4

;
使用帮助 返回顶部