| Objectives: Through observing the pathologic change in intracranialaneurysm, and detect the expression level of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β), interleukin-6(IL-6) and nuclear factor-κB (NF-κB) inintracranial aneurysm. To investigate the correlation with clinical features. Thepurpose is providing clues for the mechanism of development, growth andrupture of intracranial aneurysm.Methord: Collecting partial aneurysm excision after clipping of it incraniotomy operation I acquired16clinical instances as the experimentalgroup since December2010to October2011in The Second Hospital of HebeiMedical University. The control group came from homeochronous patientswithout vascular diseases proved by CTA or MRI. The normal artery includedSuperficial temporal artery10instances,anterior cerebral artery and middlecerebral artery a total of9cases. The premise of obtaining above samples isthe security of patients life and operation. After general observation under thenaked eye, all the samples was doused in10%solution of formalin in12hoursin vitro. After routain HE staining and immunohistochemistry staining ofTNF-α,IL-1β,IL-6,NF-κB, observe the different colouring parts betweennormal and aneurysm vessel wall under the light microscope; detect theirexpression intensity in using of immunohistochemical analysis software.Analysis the expression of TNF-α, IL-1β, IL-6, NF-κB, combined with clinicalfeatures and lesion characteristics, investagate the correlation between TNF-α,IL-1β,IL-6,NF-κB and intracranial aneurysm.Results:1General observation under the naked eye10cases of normal superficial temporal artery are all pink white, good elasticity, texture moderate.9cases of normal anterior cerebral and middlecerebral artery branch are pink and white or pale white, good elasticity, texturemoderate.16cases of aneurysm specimens are mostly purple-brown or purple,and some tumor wall is yellow-white, their texture are uneven and some ofthem stiff and tough, and some soft. Mostly there are atherosclerotic plaquethat attached to the lining of aneurysm, thrombus composition appears in partof the aneurysm intracavity, and some of them are organized and calcified.The aneurysm wall is different in thickness, generally the top is thinner thanthe base, and only one layer of translucent membranous tissue remains in mostaneurysm wall of the samples.2under the H&E Staining light microscopyThe structure of each layer is normally exist in the arterial vessal wall ofthe control group, and no significant inflammatory cell infiltration. In contrast,the aneurysm wall of the experimental group has largely been missing fromthe three-tier structure of the normal artery wall: the endometrium becomethinning, the endothelial cells are significantly reduced, and some evendisappear completely, part of them has been stripped and protrude into thelumen in dissociation, thrombus and organized thrombus are visible, internalelastic membrane is disrupted or disappeared; the medial smooth muscle layeris atrophy, and plenty of smooth muscle cells are reduced even disappeared,replaced by a great quantity of fibrous tissue, and the proliferous fibersarranged in disorder, part of the aneurysm wall present homogeneous hyalinedegeneration or mucoid degeneration; the outer layer is thin and the tissuearranges loosely. There are numerous inflammatory cells infiltrated in themedium and outer membran. Arteriosclerosis-like changes are visible inmajority of the aneurysm wall.3Immunohistochemical resultsThe cytoplasm, interstitium or nucleus present brown or tan if theexpression of TNF-α, IL-1β, IL-6, NF-κB is positive. In the control group,there is no significant expression of TNF-α, IL-1β, IL-6, NF-κB in each layerof the wall; while in the experimental group, positive expression is visible in every layer of the aneurysm wall, and mainly concentrated in theendotheliocyte, macrophagocyte and smooth muscle cell of intima and tunicamedia. The positive expression intensity of TNF-α, IL-1β, IL-6, NF-κB issignificantly higher in the artery wall of cerebral aneurysm than the normalone. Adopt SPSS13.0statistical analysis, there is statistically significance(P<0.05) in expression differences of TNF-α, IL-1β, IL-6, NF-κB between thecontrol group and experimental one, and in the aneurysm group there exists acertain positive correlation among their expression intensity.Conclusion:1The primary pathologic alternation is the endothelium destrucytion andinflammatory reaction of the vessel wall in the process of the intracranialaneurysm formation, and what followed is the serious injury of the matrixstructure and smooth muscle cells. Inflammatory reaction exists in each layerof the aneurysm wall, and it is the endothelial cells, smooth muscle cells,macrophages and lymphocytes that involved in it. Endothelial cells decreaseobviously even to disappear, and internal elastic membrane is disrupted ordisappeared; smooth muscle cells has a significant reduction and replaced byproliferous fibrous tissue, and smooth muscle layer atrophy significantly; atthe same time the structure of outer membrane is loose; there areatherosclerosis and thrombotic components in most of the aneurysm cavity; allthe evidence above support that there is relationship between the aneurysmformation and the degenerative pathologic alternation of the arterial wall.2Positive expression of TNF-α, IL-1β, IL-6and NF-κB as inflammatorycytokines can be detected in there layer of the intracranial aneurysm wall, andis mainly expressed in the intima and media; in aneurysm group, theexpression intensity is significantly higher than that in the control group; andthere exists some positive correlation among the expression intensity ofTNF-α, IL-1β, IL-6and NF-κB; which prompt that TNF-α, IL-1β, IL-6andNF-κB may participate in the formation and rupture of intracranial aneurysmscollectively.3Probably, TNF-α, IL-1β, IL-6, and NF-κB play an important role in the development of intracranial aneurysms. It may be effective to inhibit theoverexpression of them in reducing the incidence of intracranial aneurysms,which provide a new idea in the prevention and treatment of intracranialaneurysms. |
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