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作 者:王淑娟[1] 许亚茹[2] 元小冬[1] 李静[1] 杨娜[1]
机构地区:[1]华北煤炭医学院附属开滦医院神经内科,唐山063000 [2]华北煤炭医学院附属医院医院感染管理科,唐山063000
出 处:《免疫学杂志》2010年第11期956-961,共6页Immunological Journal
摘 要:目的研究尿酸异常与纤维蛋白原(fibrinogen,Fg)Bβ链-854G/A、-455G/A、-249C/T、-148C/T、448G/A和Bcl-1G/A位点基因多态性及其血浆Fg含量和聚合功能表达的关系。方法选取开滦集团离退休职工1386人,均抽取清晨空腹静脉血测定血生化、尿酸(UA)、血浆Fg浓度和纤维蛋白单体聚合反应速率(FMPV)、FMPV/Amax等反映Fg聚合功能的指标,并检测FgBβ链6个位点基因多态性。依据尿酸值将人群分为高尿酸血症组与正常尿酸组,探讨尿酸异常与Fg的关系。结果高尿酸与否人群FgBβ各多态性位点等位基因和基因型频率分布差别无统计学意义(P>0.05);在-854GG型、-455GG型、Bcl-1GG型人群中FMPV/Amax,-249CT+TT型人群中Fg浓度、FMPV、FMPV/Amax,-148CC型、448GG型人群中Fg浓度、Amax均为高尿酸血症组低于正常尿酸组(P<0.05);以有无高尿酸为因变量的Logistic回归分析,依次筛选出肌酐、性别、高血压病、体重指数、年龄、FMPV/Amax等指标。结论尿酸可以影响FgBβ链6个基因多态性位点对于血浆Fg含量和分子活性功能表达的调控作用;高尿酸血症与脂代谢异常及其引发的慢性炎症反应等因素共同作用可导致脑梗死的发病。This article is aimed to study the correlation of serum uric acid(UA) with Bβ-854G/A,-455G/A,-249C/T,-148C/T,448G/A,Bcl-1G/A six gene polymorphisms of fibrinogen(Fg),plasma Fg concentration,and molecular reactivity.In our research,1 386 subjects fromKailuan Corporation were enrolled with study method of clustersampling.All subjects were phlebotomized at the early morning to measure UA,Fg concentration,fibrin monomer polymerized velocity(FMPV),absorbance maximum(Amax) and FMPV/Amax rate,while the six gene polymorphisms were detected too.Based on the UA value,the subjects were divided into high uric acid group and normal uric acid group.The results indicated that no different genotypes and alleles frequencies of six sites were found in high UA and normal UA groups(P 0.05);in the high UA group,we found that the FMPV/Amax of wild genotypes Bβ-854,Bβ-455 and Bcl-1 people,the Fg concentration,FMPV,FMPV/Amax of Bβ-249 mutated genotype people,the Fg concentration and Amax of Bβ-148 and Bβ448 wild genotype people were all lowerthan those of the normal UA group(P 0.05).In logistic regression analysis of correlative factors to UA,Creatinine,gender,hypertension,body mass index,age and FMPV/Amax were selected in turn(P 0.01).This study shows that UA can affect the regulatory action of Fg gene polymorphisms on the expression of Fg concentration and molecular reactivity.Furthermore,hyperuricaemia,combined with abnormal lipid metabolismand chronic inflammation of which caused,can lead to onset of cerebral infarction.
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