期刊文献+

缺氧诱导因子-1a和血清促红细胞生成素在脑出血患者中的表达及意义 被引量:3

A correlation study on expression of hypoxia inducible factor-1a and serum erythropoietin in cerebral hemorrhagical perifocus
下载PDF
导出
摘要 目的探讨脑出血灶周缺氧诱导因子-1a(hypoxia inducible factor-1a,HIF-1a)和血清促红细胞生成素(erythropoietin,EPO)的表达及意义。方法采用免疫组化法、放射免疫法分别检测31例脑出血灶周脑组织中HIF-1a及血清EPO的表达,并与健康对照组17例比较。结果31例脑出血灶周HIF-1a表达率为41.94%,与对照组比较差异有统计学意义(P<0.01);HIF-1a随出血量增加表达随之升高,大、中量组与对照组及大量组与小量组比较差异有统计学意义(P<0.05或P<0.001)。EPO随出血量增加表达随之降低,但均高于对照组,且差异有统计学意义(P<0.05或P<0.001);大、中量组与小量组比较差异有统计学意义(P<0.01)。HIF-1a随手术时间推迟表达升高,而EPO表达和病程无相关性。HIF-1a和EPO呈负相关(r=-0.432,P<0.05)。结论脑出血后HIF-1a、EPO的表达有明显改变,在灶周低氧所致血管新生过程中可能起重要作用。 Objective To explore expression and significance of hypoxia inducible factor-1a (HIF-1a)and serum erythropoietin (EPO) in cerebral hemorrhagcal perifocus. Methods Expression of HIF-1a and serum EPO were assessed by immunohistochemical straining and radioimmunoassay in 31 cases with hypertensive hemorrhage and were compared to the normal group eontaining 17 cases. Results In 31 cases of hypertensive hemorrhage,the expressional rate of HIF-1a was 41.94 %. There was significant difference compared to normal group ( P 〈0.01 ). Expression of HIF-1a got higher as the volume of hemorrhage increased. There were significant difference between the massive-intermediate volume group and the control group, and between the massive volume group and the small volume group (P 〈 0.05 or P 〈 0. 001 ). Expression of EPO got lower as the volume of hemorrhage increased, but were all higher than those in the control group. There was significant difference between the massive to intermediate volume group and the small volume group ( P 〈 0.01 ). Expression of HIF-1a got higher with the delay of operation time. There was no correlation between the expression of HIF-1a and course of illness. There was a negativly correlation between HIF-1 a and EPO ( r = - 0.432, P 〈 0.05 ). Conclusions Expression of HIF-1a and EPO changed significantly after cerebral hemorrhage. It may have important effect on the course of pefifocus leading to vasoneogenesis.
出处 《中风与神经疾病杂志》 CAS CSCD 北大核心 2008年第1期30-32,共3页 Journal of Apoplexy and Nervous Diseases
关键词 缺氧诱导因子-1a 促红细胞生成素 脑出血 Hypoxia inducible factor-1 a Erythropoietin Cerebral hemorrhage
  • 相关文献

参考文献2

二级参考文献12

  • 1Pulsinelli WA,Brierley JB.A new model of bilateral hemispheric ischemia in the unanesthetized rat[J].Stroke,1979,10(3):267-272. 被引量:1
  • 2Siren AL,Fratelli M,Brines M,et al.Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress[J].Proc Nad Acad Sci USA,2001,98(7):4044-4049. 被引量:1
  • 3Digicaylioglu M,Lipton SA.Erythropoietin-mediated neuroprotection involves cross-talk between Jak2 and NF-kB signalling cascades[J].Nature,2001,412(6487):641-647. 被引量:1
  • 4Dawson TM.Preconditioning-mediated neuroprotection through erythropoietin [J].Lancet,2002,359(9301):96-97. 被引量:1
  • 5Brines ML,Ghezzi P,Keenan S,et al.Erythropoietin crosses the blood-brain barrier to protect against experimental brain injury[J].Proc Natl Acad Sci USA,2000,97(19):10526-10531. 被引量:1
  • 6Sugawara T,Fujimura M,Morita-Fujimura Y,et al.Mitochondrial release of cytochrome c corresponds to the selective vulnerability of hippocampal CA1 neurons in rats after transient global cerebral ischemia[J].The Journal of Neuroscience,1999,19(22):1-6. 被引量:1
  • 7Marsden VS,O'Connor L,O'Reilly LA,et al.Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome[J].Nature,2002,419(6907):634-637. 被引量:1
  • 8Tamatani M,Mitsuda N,Matsuzaki H,et al.A pathway of neuronal apoptosis induced by hypoxia/reoxygenation:roles of nuclear factor-kappaB and Bcl-2[J].J Neurochem,2000,75(2):683-693. 被引量:1
  • 9Shimizu S,Narita M,Tsujimoto Y.Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC[J].Nature,1999,399(6735):483-487. 被引量:1
  • 10Wen TC,Sadamoto Y,Tanaka J,et al.Erythropoietin protects neurons against chemical hypoxia and cerebral ischemic injury by up-regulating Bcl-xL expression[J].J Neurosci Res,2002,67(6):795-803. 被引量:1

共引文献23

同被引文献98

引证文献3

二级引证文献5

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