南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (08): 1189-.

• • 上一篇    下一篇

基质金属蛋白酶-9在后交通动脉瘤瘤周蛛网膜中的表达及临床意义

冯文峰,王刚,张国忠,李伟光,李明洲,何小艳,张龙,漆松涛   

  • 出版日期:2013-08-20 发布日期:2013-08-20

Expression of matrix metalloproteinase-9 in the arachnoid membrane around posterior communicating artery aneurysms

  • Online:2013-08-20 Published:2013-08-20

摘要: 目的初步探讨基质金属蛋白-9(MMP-9)在后交通动脉瘤瘤周蛛网膜中的表达及意义。方法选取南方医科大学南方医
院2010年11月~2011年11月手术切除的颅内动脉瘤标本12例作为颅内动脉瘤组,并选取同期行海绵状血管瘤手术或颞叶癫痫
手术患者后交通动脉起始部附近蛛网膜组织6例作为对照组。标本行常规HE染色,并采用Envision法行免疫组化染色,比较
组间MMP-9的阳性表达情况。结果HE染色提示动脉瘤瘤周的蛛网膜存在一定的组织破坏,表现为蛛网膜结构松散,与血管壁
之间的连接程度下降,局部存在脱离现象。动脉瘤组瘤周蛛网膜中MMP-9阳性表达均高于照组,具有统计学意义(P<0.05)。
动脉瘤组内蛛网膜中MMP-9的阳性表达强度较血管壁弱,具有统计学意义(P<0.05);动脉瘤组内不同年龄、Hunt-Hess分级的
MMP-9表达情况无显著性差异。结论动脉瘤瘤周蛛网膜中MMP-9表达明显增加预示着细胞外基质的溶解,破坏蛛网膜对血
管壁的保护作用,可能与后交通动脉瘤的形成有重要关系。

Abstract: Objective To investigate the expression of matrix metalloproteinase-9 (MMP-9) in the arachnoid membrane around
posterior communicating artery aneurysms. Methods Twelve patients with posterior communicating artery aneurysms
undergoing surgical intervention in our hospital between November, 2010 and November, 2011 were enrolled as the case
group along with 6 concurrent patients with severely head trauma or epilepsy as controls. The expression of MMP-9 in the
aneurysmal walls and the arachnoid membrane was examined in immunohistochemistry, and HE staining and Sirus red
staining were performed to examine the pathological changes. Results The perianeurysmal arachnoid membrane showed
tissue destruction and disruption of the connections between the membrane and the artery wall with local detachment.
Compared with that in the control group, the level of MMP-9 in the arachnoid membrane was significantly higher in the case
group (P<0.05), but significantly lower than that in the aneurysm wall within the same sample (P<0.05). No differences were
found in the levels of MMP-9 in the aneurysm patients with different ages or Hunt-Hess scale scores. Conclusion MMP-9 is
closely related with the formation of posterior communicating artery aneurysms by causing degradation of extracellular
matrix of the vascular wall and the arachnoid membrane.