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目的 探讨细菌性颅内动脉瘤 (BIAs)的发病机理。方法 用地高辛标记的 72 和92 KDaIV型胶原酶 (MMP 2和MMP 9)及其组织抑制因子 (TIMP) 1、TIMP 2反义RNA探针与BIAs(n =2 )和正常脑动脉组织 (n =6 )进行原位杂交 ,定位产生它们的细胞。并用正义RNA探针进行阴性对照。结果 2份感染性颅内动脉瘤标本中均见MMP 9mRNA阳性杂交信号。且在内膜 ,尤其是相当于内弹力层部位 ,阳性杂交信号密集存在。动脉瘤壁内弹力层消失。阳性杂交信号定位于单核细胞、成纤维细胞和平滑肌细胞。正常脑动脉标本中未发现MMP 9mRNA阳性杂交信号。在BIAs和正常脑动脉组织中未发现MMP 2、TIMP 1和TIMP 2的mRNA阳性杂交信号。结论 感染因素引起炎性细胞浸润 ,表达MMP 9mRNA增多 ,导致内弹力层断裂、消失 ,甚至动脉壁全层结构的破坏 ,从而引发BIAs形成。
Objective To investigate the pathogenesis of bacterial intracranial aneurysms (BIAs). Methods Digoxin-labeled 72 and 92 KDa type IV collagenase (MMP 2 and MMP 9) and their tissue inhibitor of metalloproteinase (TIMP) 1 and TIMP 2 antisense RNA probe were used to detect the expression of Bcl-2 and Bcl-2 in normal cerebral arteries n = 6) for in situ hybridization to locate the cells that produced them. Negative controls were also performed with sense RNA probes. Results The MMP 9 mRNA positive hybridization signals were found in 2 infected intracranial aneurysms. And in the endometrium, especially in the region corresponding to the inner elastic layer, positive hybridization signal intensive presence. Aneurysm wall elastic layer disappears. Positive hybridization signals are localized to monocytes, fibroblasts and smooth muscle cells. No MMP 9 mRNA positive hybridization signal was found in normal cerebral arteries. No mRNA positive hybridization signals of MMP 2, TIMP 1 and TIMP 2 were found in BIAs and normal cerebral arteries. Conclusions Infection factors cause infiltration of inflammatory cells and increase expression of MMP 9 mRNA, which leads to the rupture and disappearance of the internal elastic layer and even the destruction of the entire layer structure of the arterial wall, thereby triggering the formation of BIAs.