TNF-α-308G>A and IL-6-174G>C polymorphisms in Tunisian patients with coronary artery disease

被引:27
作者
Ghazouani, Lakhdar [1 ]
Khalifa, Sonia Ben Hadj [1 ]
Abboud, Nesrine [1 ]
Ben Hamda, Khaldoun [2 ]
Ben Khalfallah, Ali [3 ]
Brahim, Nsiri [1 ]
Almawi, Wassim Youssef [4 ]
Mahjoub, Touhami [1 ]
机构
[1] Fac Pharm Monastir, Res Unit Biol & Genet Canc Haematol & Autoimmune, Monastir 5000, Tunisia
[2] CHU Fattouma Bourguiba Hosp Ctr, Dept Cardiol, Monastir, Tunisia
[3] Menzel Bourguiba Hosp Ctr, Bizerte, Tunisia
[4] Arabian Gulf Univ, Coll Med & Med Sci, Manama, Bahrain
关键词
Interleukin-6; TNF-alpha; Polymorphisms; Coronary artery disease; Inflammatory cytokine; NECROSIS-FACTOR-ALPHA; MYOCARDIAL-INFARCTION; PROMOTER POLYMORPHISMS; INTERLEUKIN-6; GENE; PLASMA-LEVELS; NO ASSOCIATION; INSULIN-RESISTANCE; SOLUBLE FRACTION; RISK; INFLAMMATION;
D O I
10.1016/j.clinbiochem.2010.05.005
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objective: Our aim was to evaluate the contribution of tumor necrosis factor (TNF)-alpha -308G>A and interleukin (IL)-6 -174G>C gene promoter variants to the presence of coronary artery disease (CAD) in Tunisians. Design and methods: Study subjects comprised 418 angiographically proven CAD patients and 406 age-, gender-, and ethnic origin-matched controls. Genotyping was performed using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Results: There were no significant differences in the allelic distribution of TNF-alpha -308A (19.6% vs. 19.0%, P = 0.73), and IL-6 -174C (15.6% vs. 14.3%, P = 0.47) promoter polymorphisms between CAD patients and control subjects, respectively. In addition, single locus analysis revealed no differences in genotype frequencies between the two study groups, and the combined distribution of both genotypes did not differ significantly between controls and CAD patients (P > 0.05). Conclusion: There is no allelic or genotypic association of TNF-alpha -308G>A and IL-6 -174G>C promoter polymorphisms with CAD in Tunisians, thereby confirming an ethnic-selective contribution of both gene variants to CAD presence. (C) 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1085 / 1089
页数:5
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