摘要
目的 探讨新疆维汉两民族冠心病患者载脂蛋白AI基因启动子嘌呤置换突变限制性片段长度多态性。方法 用酚氯仿抽提核酸法从外周血白细胞中分离DNA ,用多聚酶链式反应 限制性片段长度多态性 (PCR RFLP)方法对新疆维汉两民族 10 7例冠心病患者和 5 0例对照组进行载脂蛋白AI(ApoAI)基因启动子嘌呤置换突变限制性片段长度多态性 (- 75bpG/A和 +83bpC/T)MspⅠ酶切研究。结果 ①M1- (- 75bp位点为GA或AA)等位基因频率在冠心病组为 0 49,与对照组 (0 30 )比较有显著差别 (P <0 0 5 )。冠心病组中稳定性心绞痛 (SAP)、不稳定性心绞痛 (UAP)和心肌梗死 (MI)M1-等位基因频率分别为 0 37、0 5 4和 0 5 2 ,相互间比较无显著性差异 (P >0 0 5 )。M1-与冠心病其他危险因子一起作Logistic回归分析 ,M1- (OR =3 74,P <0 0 5 )为冠心病的危险因子之一。②M2 - (+83bp位点为CT或TT)等位基因频率在冠心病组为 0 11,与对照组 (0 12 )比较无显著差异 (P <0 0 5 )。SAP、UAP和MI中M2 -等位基因频率分别为 0 0 9、0 11和 0 12 ,相互间及与对照组比较均无显著性差异 (P >0 0 5 )。M2 -与冠心病其他危险因子一起做Logis tic回归分析 ,M2 - (OR =0 .80 ,P >0 0 5 )与冠心病无相关。结论 新疆乌鲁木齐维汉两民?
Objective To analyze relationship between polymorphism at Apolipoprotein (Apo) AI gene and risk for coronary artery disease (CAD). Methods A total of 107 patients (mean age 56±11 years) diagnosed as having stable angina pectoris (SAP) (23 cases ), unstable angina pectoris (UAP)(23 cases) or myocardial infarction (MI)(61 cases) were prospectively evaluated . DNA was obtained from the 107 patients and 50 controls. In order to determine Apo AI genotypes at two polymorphic sites (G/A at-75 bp, and C/T at +83 bp ), DNA was PCR amplified and digested with Msp Ⅰ. Results The frequency of carriers of rare allele at the -75 bp site(M1-) was 0.49 in cases and 0 30 in controls ( P<0 05 ). The frequencies of the M1-allele among patients with SAP, UAP, MI and controls were 0 37(vs.controls, P>0 05 ), 0 54( P<0 05 ), 0.52( P<0 05 ) and 0.30, respectively. The frequencies for carriers of rare allele at +83 bp polymorphism (M2) was observed among patients with SAP (0 09, vs. controls, P>0.05 ), UAP (0.11, P>0 05 ) or MI(0 12, P>0 05 ) and controls (0 12). There was an increase in the frequency of M1-allele in patients with SAP to UAP or MI(0.37 vs. 0 54 vs. 0 52; all P>0 05 ) and M1 polymorphism as a risk factor for CAD (OR=3 74, P<0 05 ). In +83 bp polymorphism there was no difference in the allelelic frequencies in cases and controls (0.11 vs. 0 12; P>0.05 ). There was no significant difference in the frequency of M2- allele in patients with SAP to UAP or MI( 0.09 vs. 0.11 vs. 0 12 ; all P>0.05 ) and M2 polymorphism is not as a risk factor for CAD(OR=0.80, P>0.05 ). Plasma lipoprotein values in patients with allele M1- and M2- had no difference levels than those homozygous for M1+ and M2+ ( P>0.05 ). Conclusion M1 polymorphism (M1-) may be as a risk factor for CAD and M2 polymorphism ( M2- ) not as a risk factor for CAD.
出处
《岭南心血管病杂志》
2001年第3期155-159,共5页
South China Journal of Cardiovascular Diseases
