Expression of NF-κ3, MCP-1 and MMP-9 in a Cerebral Aneurysm Rabbit Model

被引:26
作者
Liu, Yan Fei [1 ]
Zhang, Yongqiang [2 ]
Dai, Dawei [3 ]
Xu, Zheng [1 ]
机构
[1] Mudu Peoples Hosp Suzhou, Dept Neurosurg, Suzhou, Peoples R China
[2] Chinese Armed Police Force, Hosp Hebei Prov Corps, Dept Neurosurg, Shijiazhuang, Hebei, Peoples R China
[3] Second Mil Med Univ, Changzheng Hosp Shanghai, Dept Neurosurg, Shanghai, Peoples R China
关键词
NF-KAPPA-B; INTRACRANIAL ANEURYSM; MATRIX; MATRIX-METALLOPROTEINASE-9; MEDIATOR; PATHWAY;
D O I
10.1017/S0317167100016589
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: We explored the early expression of NF-kappa B, MCP-1 and -MMP 9 in a rabbit carotid aneurysm model, and investigated the possible mechanism of aneurysm. Methods: Twenty four adult New Zealand rabbits were divided into four groups. Normal control (Group A); Rabbits received elastase induction for I, 2 3 weeks (Group B, C and D respectively); Hematoxylin-Eosin stains were performed for observation. The mRNA and protein expression of NF-kappa B, MCP-1 and MMP-9 were analyzed using RT-PCR and irnmunohistochemical methods. Results: The expression of NF-kappa B and MCP-1 reached their peaks after induction for one week, then decreased. Their expression in week 1 and week 2 had no statistical difference. The expression of MMP-9 increased after induction. We observed the highest expression at week 3. As the induction time increased, the number of smooth muscles reduced. Endothelial cells were damaged; the aneurysm wall elastic layer was damaged. Conclusion: Activation of NF-kappa B may be one of the initiating factors contributing to the occurrence and development of cerebral aneurysm. MCP-1 induced macrophage adhesion and infiltration in the artery wall of cerebral aneurysms, and contributed to the occurrence and development of brain aneurysm. Damage to elastic fibers is one of the key factors for aneurysm formation. Increased infiltration of inflammatory cells and the secretion of MMP-9 are the main reasons for elastic fiber damage.
引用
收藏
页码:200 / 205
页数:6
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