中华神经外科杂志
中華神經外科雜誌
중화신경외과잡지
Chinese Journal of Neurosurgery
2008年
7期
521-524
,共4页
郭予大%林晓风%邹朝霞%游潮
郭予大%林曉風%鄒朝霞%遊潮
곽여대%림효풍%추조하%유조
颅内动脉瘤%CD68%c-Jun%MMP-9%发病机制
顱內動脈瘤%CD68%c-Jun%MMP-9%髮病機製
로내동맥류%CD68%c-Jun%MMP-9%발병궤제
Intracranial aneurysm%CD68%c-Jun%MMP-9%Pathogenesis
目的 探讨颅内动脉瘤组织超微结构及MMP-9过度表达的相关调控机制.方法 观察颅内动脉瘤标本和正常脑血管的血管壁细胞外基质的形态学变化,检测脑血管壁组织内的CD68、MMP-gmRNA表达水平及c-Jun免疫活性,进行相关统计学分析.结果 电镜下见颅内动脉瘤血管壁的内皮细胞、平滑肌细胞凋亡和细胞外基质(ECM)破坏,CD68在颅内动脉瘤组织内14.60±1.72/高倍视野,正常脑血管壁内未见CD68阳性表达(P<0.01);c-Jun免疫活性在颅内动脉瘤组织内为1.92±051,正常脑血管壁内为0.17±0.41(P<0.01);动脉瘤组织中MMP-9mRNA的表达是正常对照的10.06倍(P<0.01);CD68和MMP-9mRNA之间呈显著正相关(r<,1>=0.931);颅内动脉瘤组织内c-Jun和MMP-9mRNA之间呈显著正相关(r<,2>=0.818).结论 颅内动脉瘤瘤壁组织中阳性表达的CD68可能通过激活c-Jun进而诱导MMP-9的大量表达破坏ECM参与颅内动脉瘤的发病机制.
目的 探討顱內動脈瘤組織超微結構及MMP-9過度錶達的相關調控機製.方法 觀察顱內動脈瘤標本和正常腦血管的血管壁細胞外基質的形態學變化,檢測腦血管壁組織內的CD68、MMP-gmRNA錶達水平及c-Jun免疫活性,進行相關統計學分析.結果 電鏡下見顱內動脈瘤血管壁的內皮細胞、平滑肌細胞凋亡和細胞外基質(ECM)破壞,CD68在顱內動脈瘤組織內14.60±1.72/高倍視野,正常腦血管壁內未見CD68暘性錶達(P<0.01);c-Jun免疫活性在顱內動脈瘤組織內為1.92±051,正常腦血管壁內為0.17±0.41(P<0.01);動脈瘤組織中MMP-9mRNA的錶達是正常對照的10.06倍(P<0.01);CD68和MMP-9mRNA之間呈顯著正相關(r<,1>=0.931);顱內動脈瘤組織內c-Jun和MMP-9mRNA之間呈顯著正相關(r<,2>=0.818).結論 顱內動脈瘤瘤壁組織中暘性錶達的CD68可能通過激活c-Jun進而誘導MMP-9的大量錶達破壞ECM參與顱內動脈瘤的髮病機製.
목적 탐토로내동맥류조직초미결구급MMP-9과도표체적상관조공궤제.방법 관찰로내동맥류표본화정상뇌혈관적혈관벽세포외기질적형태학변화,검측뇌혈관벽조직내적CD68、MMP-gmRNA표체수평급c-Jun면역활성,진행상관통계학분석.결과 전경하견로내동맥류혈관벽적내피세포、평활기세포조망화세포외기질(ECM)파배,CD68재로내동맥류조직내14.60±1.72/고배시야,정상뇌혈관벽내미견CD68양성표체(P<0.01);c-Jun면역활성재로내동맥류조직내위1.92±051,정상뇌혈관벽내위0.17±0.41(P<0.01);동맥류조직중MMP-9mRNA적표체시정상대조적10.06배(P<0.01);CD68화MMP-9mRNA지간정현저정상관(r<,1>=0.931);로내동맥류조직내c-Jun화MMP-9mRNA지간정현저정상관(r<,2>=0.818).결론 로내동맥류류벽조직중양성표체적CD68가능통과격활c-Jun진이유도MMP-9적대량표체파배ECM삼여로내동맥류적발병궤제.
Objective To investigate the ultrastructural and the regulation mechain of MMP-9's overexpression in the patiens with intraeranial aneurysms. Method The uhrastructure of aneurysms and vessel were observed with transmission electron microscope,the expression of CD68 and c-Jun and the gene expression levels of MMP-9 mRNA in tissue samples of 15 cerebral aneurysms and 6 cases from normal brain vessel without vascular disorder were measured by immunohistochemical SP method and real time TaqRT-PCR quantify method respectively. Results The damage of endothelial cell was found in aneurysms,what's more, the media smooth muscle cell apeptosis was found, ECM was damaged obviously. The expression levels of CD68 and c-Jun, MMP-gmRNA were significantly upregulated in aneurysms compared with that of the normal artery( 14.60 ± 1.72/high multiple vision versus 0, 1.92 ± 051 versus 0.17 ±0.41,10.06fold. P <0.01 respectively). There were a significant parallel tendency between CD68, c-Jun and MMP-gmRNA respectively. Conclusions The positive expression of CD68 in intracranial aneurysm may induct a overexpression of MMP-9 through activation of CD68 ,and the overe.xpression of MMP-9 destroy ECM to take part in the pathogenesis of the intracranial aneurysm.
