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Relationship Between Coronary Atherosclerotic Plaque Stability And Inflammatory Factors And NF-κB

Posted on:2010-06-30Degree:MasterType:Thesis
Country:ChinaCandidate:S W ShiFull Text:PDF
GTID:2144360275992476Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Background:The chronic inflammatory response by cell-mediated has been confirmed more association with atherosclerosis in the formation and development. Inflammatory response in which both plays a very important role,such as from the early endothelial chemokine expression,leukocyte aggregation and endothelial cells to soak into its next to the foam cell formation,the emergence of plaque development, rupture,thrombosis or myocardial infarction caused by embolism.Nuclear factor-κb(NF- B) are Rel protein family members.Kranzhofer further founded that when angiotensinⅡand its receptor binded,the vascular smooth muscle cells NF- B were activatied,IL-6mRNA enhanced transcription,which induced chronic inflammatory response of vascular wall.It's suggested that angiotensinⅡ-induced vascular smooth muscle cells of the oxidation reaction,and control IL-6 expression and release,activate NF- B by oxygen free radicals.All of these Lead to the chronic inflammatory response of vascular wall and promote atherosclerosis.Besides,cytomegalovirus,chlamydia pneumoniae infection also can activate NF- B,so that make vascular endothelial cells and smooth muscle cells express adhesion molecules,inflammatory mediators and growth factors.At the next-mediated adhesion molecule,monocyte and endothelial cell adhesion to subendothelial migration,inflammatory mediators and growth factor mediate chronic inflammatory response of vascular wall and smooth muscle cell proliferation and migration to the intima,all of those promote the formation of of atherosclerosis.Based on the above situation,this study aims to explore the role of plasma inflammatory cytokines and NF- B in the paitents with coronary heart disease.And to observe the Relevance between the role of these factors and stability of coronary atherosclerotic plaque.And provide preliminary theoretical basis for research of new drugs which can block the specificity of inflammatory factor binding and inhibite of its pro-inflammatory role,provide the basis for clinical diagnosis and treatment of coronary heart disease.Methods:We detected the OD value of plasma IL-10,IL-17,IL-18,hs-CRP, TNF-αby ELISA.Strictly in accordance with operation instructions Kit.We use CURVE-EXPERT 1.3 software converted into the concentration level of these factors. We checked the level of peripheral blood lymphocytes NF-?B by fluorescence quantitative PCR method with ABI7000.A11 data were analysised by software SPSS 17.0,P value<0.05 as statistically significant,P value<0.01 as significant difference.Results:①The level of these factors in the CHD group were significantly increased compared with control group(P<0.01).②The level of the above factors are also significant difference among the three groups of patients with coronary heart disease(P<0.01).③IL-10 as only one protective factor which can lower atherosclerosis risk,and its expression in coronary heart disease groups can significantly increased,when stable plaques to change unstable plaques progress,even rupture.Conclusion:①The expression of those factors were related with the degree of atherosclerosis,which through the induction of the each other are participated in the incidence and development of coronary heart disease.②IL-10 as only one protective factor which can lower atherosclerosis risk,and its expression in coronary heart disease groups can significantly increased,when stable plaques to change unstable plaques progress,even rupture.But its expression is still not be enough to prevent plaque formation,Progress even rupture.③The expression level of NF-κB in peripheral blood may become a marker of plaque stability and as a sensitive indicator which can response to the severity of CHD.A sudden increase in its level may prompt severe myocardial ischemia,injury,even myocardial infarction.
Keywords/Search Tags:Coronary atherosclerosis, Interleukin, Hypersensitive C reactive protein, Tumor necrosis factor-α, mononuclearcell nuclear factor-kb
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