期刊文献+

脑出血后脑组织内凝血酶受体1(PAR1)的表达及其病理意义 被引量:31

Role of thrombin receptor in the pathogenesis of cerebral hemorrhage in rats
下载PDF
导出
摘要 目的 探讨脑出血后脑组织内凝血酶受体 1(PAR1)的表达规律及其意义。方法 成年大鼠分为 3组 ,分别向大脑基底节区注入全血、全血加水蛭素、或生理盐水。于注射后 6 h、2 4 h、72 h和 7d,取脑组织 ,检测脑内PAR1表达 (免疫组织化学法 )。同时 ,观察神经细胞的凋亡情况 (Tunel法 )和脑组织水含量 (干燥法 )。结果 与生理盐水对照组比较 ,脑出血后血肿周围脑组织内 PAR1免疫阳性细胞数明显升高 (P<0 .0 5 )。同时 ,脑组织内凋亡细胞数和脑组织水含量也明显增加。时效学研究显示 ,PAR1表达上调开始于脑出血后 6 h,72 h达高峰 ,7d后下降。加用凝血酶抑制剂 -水蛭素者 ,出血周围组织内 PAR1表达明显抑制 ,同时脑组织水肿和神经凋亡显著减轻。结论 脑出血后脑组织 PAR1表达增加。 PAR1高表达可能介导了脑出血后神经损伤的过程。 Objective To investigate the expression of thrombin receptor 1 (PAR1) and its role in the pathogenesis of intracerebral hemorrhage (ICH).Methods The adult rats were divided into three groups,and intracerebrally given with autologous whole blood (50μl),autologous blood plus hirudin thrombin solution (10 units),or normal saline (NS),respectively.At 6,24,72 hours and 7days after injection, the brains were taken out for detecting the PAR1 expression (Immunostaining method) and the apoptosis cell (Tunel method).The water content of brains was also assayed.Results The number of positive PAR1-immunostaining cells in the tissue surrounding hemotoma were markedly increased at 6h after ICH,peaked at 72h and decreased at 7d after ICH.At the same time,the apoptosis cells and brain water contents were also increased. However PAR1 expression, apoptotic cells and brain water content were markedly inhibited in cases of coinjection of Hirudin and blood.Conclusion PAR1 expression was upregulated during ICH.The activation of PAR1 might be involved in the pathogenesis of ICH.
出处 《中风与神经疾病杂志》 CAS CSCD 北大核心 2004年第2期100-103,共4页 Journal of Apoplexy and Nervous Diseases
基金 国家自然科学基金 (3 0 171166)
关键词 脑出血 后脑组织 凝血酶受体 PAR1 组织表达 病理分析 Thrombin receptor (PAR1) Cerebral hemorrhage Brain edema Apopotosis
  • 相关文献

参考文献8

  • 1Lee KR,Colon GP,Betz AL,et al.Edema from intracerebral hemorrhage:the role of thrombin[J].J Neurosurg,1996,84:91-96. 被引量:1
  • 2Vu TK,Hung DT,Wheaton VI,et al.Molecular cloning of a functional thrombin receptor reveals a novel protealytic mechanism of receptor activation[J].Cell,1991,64:1057-1068. 被引量:1
  • 3Weinatein JR,Gold SJ,Cunningham DD,et al.Cellular location of thrombin receptor mRNA in rat brains:expression by mesescephalic dopaminenergic neurons and codistribution with prothrombin mRNA[J].J Neurosci,1995,15:2906-2919. 被引量:1
  • 4Nath FP,Jenkins A,Medelow A,et al.Early hemodynamic changes in experimental intracerebral hemorrhage [J].J Neurosurg,1986,65:697-703. 被引量:1
  • 5Yajun Jiang,Jiming Wu,Ya Hua,et al.Thrombin-receptor activation and thrombin-induced brain edema [J].J Cereb Blood Flow and Metab,2002,22:404-410. 被引量:1
  • 6Donovan FM,Pike CJ,Cotman CW,et al.Thrombin induces apoptosis in cultured neurons and astrocytes via a pathway requiring tyrosine kinase and RhoA activities[J].J Neurosci,1997,17(14):5316-5326. 被引量:1
  • 7Gingrich MB,Junge CE,Lynboslavsky P,et al.Potentiation of NMDA receptor by the serine protease thrombin[J].J Neurosci,2000,20(12):4582-4595. 被引量:1
  • 8Moller T,Hanisch UK,Tansom BR.Thrombin-induced activation of cultured rodent microglia[J].J Neurochem,2000,75:1539-1547. 被引量:1

同被引文献332

引证文献31

二级引证文献159

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