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目的:研究血管紧张素转换酶基因插入/缺失(ACEI/D)多态性及β2肾上腺素受体基因(β2-AR+46A→G)多态性与心房颤动的相关性,寻找房颤发病的分子机制。方法:选择55例房颤患者(房颤组)及63例非房颤者(对照组),用PCR的方法检测两组ACE基因插入/缺失多态性,用RFLP法检测β2-AR+46A→G变异。结果:房颤组与对照组ACEI/D多态性缺失纯合型(DD型)、杂合子(DI型)、插入纯合型(Ⅱ)基因型频率分别为32.76%、41.8%、25.5%和19.0%、44.4%、36.5%;房颤组与对照组β2-AR+46A→G多态性Gly16纯合型、Arg16纯合型、Gly16/Arg16基因型频率分别是12.7%、17.47%、61.8%和14.3%、25.3%、60.3%;房颤组与对照组D等位基因、I等位基因分布频率为53.6%、46.4%和41.2%、58.7%;房颤组与对照组Gly16等位基因、Arg16等位基因分布频率为39.6%、60.4%和38.9%、61.1%;其中D等位基因分布频率在房颤组中较对照组明显增大;在9种不同基因型联合中发现,Gly/Arg型+DD型和Gly型+DD型的两种联合在房颤组和对照组间的分布有明显差异(P<0.05),且这两种联合基因型发病相对危险度(OR)=2.455(95%CI:1.080~5.579)。结论:D等位基因可能是房颤的易患因素;ACEDD基因型与心肌纤维化及心脏重构的关系较为紧密,β2-AR基因+46A→G多态性、ID基因型和Ⅱ基因型与心肌纤维化及心脏重构无明显相关性;β2-ARGly16等位基因与ACEDD基因型的联合可能对房颤的患病有着潜在的影响。
AIM: To investigate the association between angiotensin converting enzyme gene insertion / deletion (ACEI / D) polymorphism and β2-adrenoceptor gene (β2-AR + 46A → G) polymorphism and atrial fibrillation Molecular mechanism. Methods: Fifty-five patients with atrial fibrillation (AF) and 63 patients with non-AF (control group) were enrolled in this study. ACE gene insertion / deletion polymorphism was detected by PCR in both groups. The level of β2-AR + 46A → G mutation. Results: The frequencies of ACEI / D polymorphism in patients with atrial fibrillation and control group were 32.76%, 41.8%, 25.5%, respectively, for DD type, DI type and Homozygous type Ⅱ, And 19.0%, 44.4% and 36.5% respectively. The genotypes of Gly16, Arg16 and Gly16 / Arg16 in β2-AR + 46A → G polymorphism of AF group and control group were 12.7% and 17.47% 61.8% and 14.3%, 25.3% and 60.3% respectively. The frequencies of the allele I and allele D were 53.6%, 46.4% and 41.2%, 58.7% respectively in AF group and control group. Gly16 The distribution frequency of allele of Arg16 was 39.6%, 60.4% and 38.9%, 61.1% respectively. The distribution frequency of D allele was significantly higher in AF group than that in control group. Among the 9 genotypes, , Gly / Arg type + DD type and Gly type + DD type were significantly different between AF group and control group (P <0.05), and the relative risk of these two combined genotypes (OR ) = 2.455 (95% CI: 1.080 ~ 5.579). Conclusion: D allele may be a predisposing factor for atrial fibrillation. ACEDD genotypes are closely related to myocardial fibrosis and cardiac remodeling. The polymorphisms of β2-AR gene + 46A → G, ID genotype and Ⅱ genotype And myocardial fibrosis and cardiac remodeling no significant correlation; β2-ARGly16 allele and ACEDD genotype combinations may have a potential impact on the prevalence of atrial fibrillation.