外源性VEGF对鼠脊髓缺血再灌注后内皮抑素和脑源性神经营养因子及其受体的影响

山东大学学报(医学版)

外源性VEGF对鼠脊髓缺血再灌注后内皮抑素和脑源性神经营养因子及其受体的影响

姜丽1,于灵芝1,刘旭东2,郭兰敏3

山东大学 1. 附属济南市中心医院麻醉科，济南 250013； 2. 齐鲁医院疼痛科，济南 250012；3. 附属省立医院心外科，济南 250021

收稿日期:2007-12-17 修回日期:1900-01-01 出版日期:2008-06-16 发布日期:2008-06-16
通讯作者: 于灵芝

Effect of rrVEGF165 on serum endostatin, BDNF and its TrKB receptor after spinal cord ischemia-reperfusion injury

JIANG Li¹, YU Ling-zhi¹, LIU Xu-dong², GUO Lan-min³

1. Department of Anesthesiology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China;2. Department of Analgesia, Qilu Hospital of Shandong University， Jinan 250012, China；3. Department of Cardiac Surgery

Received:2007-12-17 Revised:1900-01-01 Online:2008-06-16 Published:2008-06-16
Contact: YU Ling-zhi

摘要/Abstract

摘要： 目的探讨重组鼠血管内皮生长因子（rrVEGF¹⁶⁵）对大鼠脊髓缺血再灌注损伤后血清中内皮抑素（ES），脑源性神经营养因子（BDNF）及脊髓组织中相应受体酪氨酸激酶B（TrkB）表达的影响。方法将Wistar大鼠48只随机分为假手术组（S组，n=8），模型组（M组，n=24）和治疗组（V组，n=16）。腹主动脉阻断90min后再开放建立脊髓缺血再灌注模型。HE染色观察脊髓组织病理学变化，ELISA法检测血清ES和BDNF水平，RTPCR法检测组织中TrkB受体mRNA表达水平。结果与模型组相比，再灌注后治疗组的病理状况得到明显改善。血清学检查以假手术组为对照值。ES水平：M组再灌注后6h开始升高（P＜0.05）并持续至7d达高峰（P＜0.01）；V组虽再灌注6?h也有升高（P＜0.05），但7d时基本维持该水平，没有进一步升高。BDNF水平：M组再灌注6h降低（P＜0.01），2?d回升至对照水平；随后再度下降，7d时降至最低，仅为对照水平的59.1%（P＜0.01）,且明显低于再灌注6h（P＜0.01）；V组再灌注6?h明显升高（P＜0.01），7d时恢复至对照水平。TrkB受体mRNA表达：M组再灌注6h有所上调但2d时回调至对照水平，并于随后继续下调,至7d时表达最低；V组则于6h、7d均保持高表达（P＜0.01），并显著高于模型组（P＜0.01）。结论外源性rrVEGF¹⁶⁵能显著降低大鼠脊髓缺血再灌注后血清ES的升高，减轻BDNF的降低，促进BDNF受体TrkB mRNA的高表达，改善缺血再灌注后的脊髓病理损伤。

关键词: TrkB受体, 大鼠, 内皮抑素, 脑源性神经营养因子, 血管内皮生长因子, Wistar, 脊髓缺血再灌注

Abstract: Objective To investigate the effect of recombinant rat vascular endothelial growth factor 165 (rrVEGF165) on serum endostatin variations and brain derived neurotrophic factor (BDNF) with its tyrosin-kinase B（TrkB）receptor mRNA expression in spinal cord tissues. Methods Forty-eight rats were randomly divided into three groups: the sham-operation group(S), the model group(M) and the treatment group of rrVEGF165(V). The spinal cord ischemia-reperfusion lesion models were established by using Naslund abdominal aorta occlusion and declamped 90 minutes later. Histopathological changes in the spinal cord were observed by hematoxylin and eosion (HE) staining. Serum endostatin and BDNF levels were determined by enzyme linked immunosorbent assay (ELISA). Expressions of TrkB receptor mRNA were determined by reversetransferent polymerase chain reaction (RTPCR). ResultsInconvertible spinal damage was model group, histopathological changes in the spinal cord of group V were remarkably improved. For serum endostatin(ES): in group M, the level of endostatin began to increase after 6h post-reperfusion and remained till day 7. In group V, ES was increased at 6?h after reperfusion but that was not maintained in the following days. Serum BDNF and expression of TrkB mRNA: in group M, serum BDNF was decreased at 6?h, then returned to the control level at day 2, but was decreased more severely at day 7 which was only about 59.1% of the control level and was significant lower than that at 6h(P＜0.05). The expression of mRNA of spinal cord TrkB receptor was up-regulated at 6?h, returned to the control level at day 2, and then kept down-regulating to the lowest level at day 7 after reperfusion. In group V, in contrast, serum BDNF was significantly increased at 6?h, then returned back to the control group at day 7, and the expression of TrkB mRNA maintained a sustainable upregulation level. ConclusionSpinal rrVEGF165 administration can alleviate the increase of ES and the decrease of serum BDNF induced by spinal cord ischemic reperfusion injury, and enhances the up-regulation of mRNA expression of TrkB receptor.

Key words: Spinal cord ischemiareperfusion, Recombinant rat vascular endothelial growth factor 165, Endostatin, Brain derived neurotrophic factor, Tyrosinkinase B receptor, Rat, Wistar

中图分类号:

R744.1

姜丽,于灵芝,刘旭东,郭兰敏 . 外源性VEGF对鼠脊髓缺血再灌注后内皮抑素和脑源性神经营养因子及其受体的影响[J]. 山东大学学报(医学版), 2008, 46(6): 586-589.

JIANG Li,YU Ling-zhi,LIU Xu-dong,GUO Lan-min. Effect of rrVEGF165 on serum endostatin, BDNF and its TrKB receptor after spinal cord ischemia-reperfusion injury [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2008, 46(6): 586-589.

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