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The association between NFKB1 -94ATTG ins/del and NFKB1A -826C/T genetic variations and coronary artery disease risk

Journal: Molecular Biology Research Communications (Vol.7, No. 1)

Publication Date:

Authors : ; ; ; ;

Page : 17-24

Keywords : Coronary artery disease; Nuclear factor κB; Polymorphism;

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Coronary artery disease (CAD) is considered as a chronic inflammatory disease initiated from early childhood. Nuclear factor κB (NF κB) and κB1A (NF κB1A) are the key regulators of inflammatory responses. The NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphisms may contribute to the development of CAD. The aim of the present study was to investigate the association of these polymorphisms with the risk of CAD. The study population included 120 patients with angiographically confirmed CAD and 100 matched controls. Genotyping of NFKB1 -94ATTG ins/del and NFKB1A -826C/T polymorphism was performed using PCR-RFLP method. Lipid level was determined by routine colorimetric methods. Statistical analysis was done by SPSS 16 software. Results indicated that the genotypic (P=0.041) and allelic (P=0.009) distribution of the NFKB1-94ATTG ins/del polymorphism was significantly different between the two groups. In the univariate analysis (ins/ins genotype as reference), the del/del genotype (OR=2.88, 95% CI=1.21-6.84, P=0.015) but not ins/del genotype (OR=1.48, 95% CI=0.83-2.64, P=0.191) was significantly associated with the increased risk of CAD. In the multiple binary logistic regression analysis, diabetes, hypertension, smoking, LDL-cholesterol, total cholesterol, HDL-cholesterol and NFKB1 -94ATTG del/del genotype were identified as significant and independent risk factors for CAD development. The distribution of genotypes and alleles of NFKB1A -826C/T polymorphism was not significantly different between the two groups. In conclusion the present study identified NFKB1 -94ATTG ins/del polymorphism but not NFKB1A -826C/T polymorphism as a significant and independent risk factor for development and severity of CAD.

Last modified: 2018-04-30 15:19:12