期刊文献+

激肽原酶对大脑中动脉缺血大鼠CGRP、RAMP1及VEGF表达的影响 被引量:4

Effect of human urinary kallidinogenase on expression of CGRP,RAMP1 and VEGF in rats suffered focal cerebral ischemia
下载PDF
导出
摘要 目的研究激肽原酶预处理对脑缺血大鼠降钙素基因相关肽(CGRP)、受体活性修饰蛋白1(RAMP1)及血管内皮生长因子(VEGF)表达的影响。方法将80只大鼠随机均分成4组,假手术组(S组)、脑缺血组(I组)、激肽原酶低剂量组(3.75×10-3PNA单位/(kg·d),I+Kal1组)、激肽原酶高剂量组(17.25×10-3PNA单位/(kg·d),I+Kal2组)。经尾静脉注射给药1周后,采用线栓法堵塞大鼠右侧大脑中动脉,建立右侧大脑中动脉缺血模型。术后24 h红四氮唑法测量脑梗死体积,使用免疫组化和Western blot法观察CGRP蛋白在海马组织内的表达及RAMP1和VEGF蛋白在皮层组织内的表达。结果与S组相比,I组大鼠脑组织CGRP、RAMP1及VEGF蛋白水平表达增加(P<0.01);与I组相比,激肽原酶高、低剂量能明显促进脑缺血大鼠脑组织CGRP、RAMP1及VEGF蛋白的表达(P<0.05),脑梗死体积缩小(P<0.05)。结论激肽原酶促进缺血脑组织内CGRP、RAMP1蛋白的表达,CGRP、RAMP1的表达可能与脑梗死后血管新生有相关性。 Objective To study the effect of human urinary kallidinogenase on expression of CGRP,RAMP1 and VEGF in rats suffered focal cerebral ischemia. Methods 80 male SD rats were randomly divided into four groups:sham operation group (S group), ischemia group (I group), low dose of kallidinogenase (3. 75 × 10 - 3 PNA / (kg ·d), I + Kal1 group) and high dose of kallidinogenase (17. 25 × 10 - 3 PNA/ (kg·d),I + Kal2 group). Each group had 20 rats. The method of line bolt blocks the right middle cerebral artery in rats was used to establish the right MCAO ischemia model after tail intravenous dosing 1 week. TTC method was used to measure the cerebral in-farction volume. Immunohistochemistry and Western blot were used to evaluate the expression of CGRP protein in the hippocampus and the expression of RAMP1 and VEGF protein in the cerebral cortex. Results Compared with the S group, the expression of CGRP,RAMP1 and VEGF increased significantly in the I group rats (P 〈 0. 01). While, compared with the I group, kallidinogenase high and low dose group can significantly reduce cerebral in-farction and markedly increase the expression of CGRP, RAMP1 and VEGF induced in cerebral ischemia 24 h after MCAO(P 〈 0. 05). Conclusion Human urinary kallidinogenase can promote the expression of CGRP and RAMP1 in ischemic brain tissues and this may be one of the mechanisms of promoting angiogenesis after cerebral infarction.
出处 《安徽医科大学学报》 CAS 北大核心 2015年第8期1063-1067,共5页 Acta Universitatis Medicinalis Anhui
基金 安徽省年度重点科研项目(编号:1301043017)
关键词 降钙素基因相关肽 受体活性修饰蛋白 1 血管内皮生长因子 激肽原酶 缺血性脑卒中 大鼠 CGRP RAMP1 VEGF human urinary kallidinogenase cerebral ischemia rat
  • 相关文献

参考文献13

  • 1Mishima T, Ito Y, Hosono K, et al. Calcitonin gene-related pep- tide facilitates revascularization during hindlimb ischemia in mice [ J ]. Am J Physiol Heart C irc Physiol, 2011, 300 ( 2 ) : H431 - 9.
  • 2Kuwasako K, Kitamura K, Nagata S, et al. Function of the cyto- plasmic tail of human calcitonin receptor-like receptor in complex with receptor activity-modifying protein 2 [ J ]. Biochem Biophys Res Commun, 2010, 392(3) :380 -5.
  • 3Font M A, Arboix A, Krupinski J, Angiogenesis, neurogenesis and neuroplasticity in ischemic stroke [ J ]. Curt Cardiol Rev, 2010, 6(3) :238 -44.
  • 4Zan L, Wu H, Jiang J, et al. Temporal profile of Src, SSeCKS, and angiogenic factors after focal cerebral ischemia: correlations with angiogenesis and cerebral edema [ J~. Neurochem Int, 2011, 58(8) :872 -9.
  • 5刘平平,苏暘力,王燕宏.尤瑞克林治疗急性期脑梗死的疗效及血清CRP的变化[J].中国实用医刊,2013,40(5):11-12. 被引量:7
  • 6Liman T G, Endres M. New vessels after stroke: postischemic neovascularization and regeneration [J].Cerebrovasc Dis, 2012,33(5) :492 -9.
  • 7Oladipupo S, Hu S, Kovalski J, et al. VEGF is essential for hy- poxia-inducible factor-mediated neovascularization but dispensable for endothelial sprouting [J]. Proc Natl Acad Sci U S A, 2011, 108(32) :13264 -9.
  • 8Ma Y, Liu W, Wang Y, et al. VEGF protects rat cortical neurons from mechanical trauma injury induced apoptosis via the MEK/ ERK pathway[J].Brain Res Bull, 2011, 86(5 -6) :441 -6.
  • 9Feng G, Xu X, Wang Q, et al. The protective effects of ealeitonin gene-related peptide on gastric mueosa injury after cerebral ischemia reperfusion in rats [J]. Regul Pept, 2010, 160(1-3) :121 -8.
  • 10Zheng S, Li W, Xu M, et al. Calcitonin gene-related peptide pro- motes angiogenesis via AMP-aetivated protein kinase, American journal of physiology [J]. Am ] Physiol Cell Physiol, 2010, 299 (6) :C1485 -92.

二级参考文献5

  • 1脑卒中患者临床神经功能缺损程度评分标准(1995)[J].中华神经科杂志,1996,29(6):381-383. 被引量:15755
  • 2Bulman N,Levy Y,Leiba R. Increased C-reactive protein levels in the polycysticorary syndrome:A marker of cardiovascular disease[J].Journal of Clinical Endocrinology and Metabolism,2004,(04):2160.
  • 3Di Napoli M,Di Gianfilippo G,Sollecito A. C-reactive protein and outcome after first-ever ischemic stroke[J].Stroke,2000,(01):238-239.
  • 4Torzewski J,Torzewski M,Bowyer DE. C reactive protein frequently colocalizeswith the terminal comp lement complex in the intima of early atherosclerotic lesion of human coronary artery[J].Arteriosclerosis,Thrombosis,and Vascular Biology,1998,(09):1386-1392.
  • 5王夏红,何文龙,赵建民.尤瑞克林治疗进展性脑梗死的疗效观察[J].中华脑血管病杂志(电子版),2010,4(5):25-27. 被引量:16

共引文献6

同被引文献37

引证文献4

二级引证文献31

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