期刊文献+

大鼠全脑缺血对再灌注海马区NO含量和Bcl-2表达的影响 被引量:9

Effects of global cerebral ischemic precondition on NO content and Bcl-2 expression in reperfusion of hippocampus
下载PDF
导出
摘要 [目的]探讨全脑缺血预处理对再灌注海马区NO含量和Bcl-2表达的影响。[方法]将72只Wistar大鼠随机分为假手术组、脑缺血组和脑缺血预处理组。假手术组:仅暴露4条血管。脑缺血组:四动脉阻断法,全脑缺血10 min。脑缺血预处理组:全脑缺血预处理3 min,再灌注24 h后再次全脑缺血10 min。所有动物均于末次脑缺血再灌注后12、24、48和72 h取脑组织海马区,硝酸还原酶法检测NO2./NO3.含量,间接反应NO含量;免疫组化方法测定海马区Bcl-2表达。[结果]与假手术比较,脑缺血组和脑缺血预处理组NO含量明显增加,脑缺血组NO含量在48 h达到高峰,72 h出现回落;脑缺血预处理组NO含量在各时间点的变化趋势不明显,与脑缺血组在48和72 h比较差异性有显著性意义(P<0.05,P<0.01)。脑缺血组和脑缺血预处理组Bcl-2表达与假手术组比较明显升高;脑缺血组Bcl-2表达24 h达到高峰,48 h开始减少;脑缺血预处理组Bcl-2表达在12 h表达开始增加,48 h达到高峰,72 h开始减少;在48和72 h,脑缺血预处理组Bcl-2表达明显高于脑缺血组(P<0.05,P<0.01)。[结论]脑缺血预处理引起的NO含量增加,可能与Bcl-2上调表达增加及高峰延迟具有一定相关性。 [ Objective] To observe the effects of global cerebral ischemic precondition on NO content and Bcl-2 expression in the reperfusion of the hippocampus. [ Methods] Seventy -two rats were randomly divided into three groups. The rats shamoperated were only explored four vessels, and global ischemia was induced by occluding four vessels for 10 minutes. In ischemic precondition group,the rats firstly subjected 3 -min global ischemia and then after 24 hours,repeated ischemia sustained for 10 minutes. At 12,24,48 and 72 h after reperfusion,the hippocampus was removed. The NO content and Bcl- 2 expression of hippocampus were respectively measured by the method of nitrate reductase and immunohistochemistry. [ Results] Comparing with sham -operated group,NO content enhanced in global ischemic or ischemia precondition group. In ischemic group,the NO content remarkably increased in 48 h and decreased in 72 h, and was significant higher at 48 h and 72 h comparing with ischemic precondition group (P 〈 0.05,P 〈 0.01 ). The expressions of Bcl -2 in global ischemic and ischemia precondition groups were higher than sham -operated group. In ischemic group, Bcl -2 expression was remarkably increasing at 24 h and decreasing at 48 h ( P 〈 0. 05, P 〈 0.01 ), but in ischemic precondition group, it increased at 48 h and decreased at 72 h. Bcl - 2 expression was significant lower in ischemic group than that in ischemic precondition group at 48 h and 72 h (P 〈0. 05 ; P 〈0.01 ). [ Conclusion] In some extent,the increase of NO content may be related with up - regulated expression of Bcl - 2 and delayed peak level in ischemic precondition.
出处 《大连医科大学学报》 CAS 2009年第6期649-652,共4页 Journal of Dalian Medical University
关键词 全脑缺血 脑缺血预处理 一氧化氮 BCL-2 海马区 global cerebral ischemia cerebral ischemic precondition nitric oxide Bcl - 2 hippocampus
  • 相关文献

参考文献14

  • 1吴燊荣,李友元,邓洪波,肖洒,王蓉.黄精多糖对老年糖尿病小鼠脑组织糖基化终产物受体mRNA表达的影响[J].中华老年医学杂志,2004,23(11):817-819. 被引量:18
  • 2Onga EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats [ J ]. Stroke, 1989,20:84.
  • 3Hillis JW, Sen S. Oxypurinol at tenuates hydroxyl radical production during ischemia/reperfusion injury of the rat cerebral cortex: An ESR study[ J]. Brain Res, 1993,628 :309 -312.
  • 4Centeno JM, Orti M,SalomJB,et al. Nitric oxide is involved n anoxic preconditioning neuroprotection in rat hippocampal lices [J]. Brain Res,1999,836 (1 -2) :62 -69.
  • 5Gonzalez - Zulueta M, Feldman AB, Klesse LJ, et al. Requirement for nitric oxide activation of p21 (ras) / extracellular egulated kinase in neuronal ischemic preconditioning [ J ]. Proc Natl Acad Sci USA, 2000,97 ( 1 ) : 436 - 441.
  • 6Ami P. Raval, Anoop Bhatt, Isabel Saul. Chronic nicotine exposure inhibits 17β - estradiol - mediated protection of the hippocampal CAI region against cerebral ischemia in female rats [ J ]. Neurosci Lett,2009 (458) :65 - 69.
  • 7Atochin DN, Clark J, Demchenko IT, et al. Rapid cerebral schemic preconditioning in mice deficient in endothelial and euronal nitric oxide synthases [ J ]. Stroke, 2003,34 (5) : 1299 - 1303.
  • 8P. Prakasa Babu,Y. Yoshida,M. Su,et al. Immunohistochemical expression of Bcl -2, Bax and cytochrome c following focal cerebral ischemia and effect of hypothermia in rat [ J ]. Neurosci Lett,2000 (291) : 196 - 200.
  • 9Willian AP, James BB. A new model of bilateral hemispheric ischemia in the unanesthetized rat. Stroke, 1979, 10 : 267 - 272.
  • 10Alvaro G. Est vez, Jacinda B. Sampson, Ying- Xin Zhuang, et al. Liposome - delivered superoxide dismutase prevents nitric oxide dependent motor neuron death induced by trophic factor withdrawal [ J ]. Free Rad Biol Med,2000(28) : 437 -446.

二级参考文献10

  • 1赵昱,李莉,尹青,罗波,李陈莉,王慧娟,马洪骏.大鼠局灶性脑缺血再灌注中nNOS源性NO对Bcl-2、Bax表达的影响[J].神经解剖学杂志,2005,21(5):539-542. 被引量:5
  • 2AM Schmidt,Shi DuYan, Jean-Luc, et al. Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfuction in diabetic vasculopathy and atherosclerosis. Circ Res, 1999, 84:489-497.
  • 3Shi Du Yan, Xi Chen, Jin Fu, et al. RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease. Nature ,1996,382:685-691.
  • 4Sasaski N,Fukatsu R, Tsuzuki K, et al.Advanced glycation end products in Alzheimer's disease and other neurodegenerative disease. Am J Pathol, 1998,153:1149-1155.
  • 5Li JJ,Dickson D, Hof PR, et al.Receptors for advanced glycosylation endproducts in human brain:role in brain homeostasis. Mol Med, 1998,4:46-60.
  • 6Ma L, Carter RJ, Morton AJ, et al. RAGE is expressed in pyramidal cells of the hippocampus following moderate hypoxic-ischemic brain injury in rats. Brain Res, 2003,21:167-174.
  • 7Renard C, Chappey O, Wautier MP, et al. Recombinant advanced glycation end product receptor pharmacokinetics in normal and diabetic rats. Molecular Pharmacology, 1997,52:54-62.
  • 8Samdani AF,Dawson TM,Dawson VL.Nitric oxide synthase in models of focal ischemia[J].Stroke,1997,28(6):1283-1288.
  • 9Longa Z,Weinstein PR,Carlson S,et al.Reversible middle cerebral artery occlusion without craniectomy in rats[J].Stroke,1989,20(1):84-91.
  • 10Tamatani M,Ogawa S,Niitsu Y,et al.Involvement of Bcl-2 family and caspase-3-like protease in NO-mediated neuronal apoptosis[J].J Neurochem,1998,71(4):1588-1596.

共引文献26

同被引文献112

引证文献9

二级引证文献44

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