ApoE基因多态性与慢性心血管疾病及患者血脂水平的相关性研究
|
摘要
目的分析载脂蛋白E(ApoE)基因多态性与慢性心血管疾病及患者血脂水平的相关性。方法采用基因芯片分析系统及生化分析仪,检测1 414例慢性心血管疾病患者(实验组)和374例健康者(对照组)ApoE基因多态性及血脂水平。结果实验组和对照组ApoE基因型分布构成比比较差异有统计学意义(P<0.05),对照组E2/3基因型构成比高于实验组。实验组总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)水平明显高于对照组,对照组高密度脂蛋白胆固醇(HDL-C)水平明显高于实验组,差异有统计学意义(P<0.05)。E2/3基因型实验组患者HDL-C水平明显高于E3/4基因型患者,而E3/4基因型患者TC、LDL-C水平明显高于E2/3基因型患者,差异有统计学意义(P<0.05)。不同ApoE基因型在脑梗死、脑出血、高血压、冠心病、2型糖尿病、脂肪肝等患者中的构成比有所差异,E3/4基因型在脑梗死、脑出血、高血压、冠心病、2型糖尿病、脂肪肝患者中所占比例高于E2/3基因型,差异有统计学意义(P<0.05)。结论 ApoE基因多态性可能是导致个体血脂水平差异的重要原因之一,也是导致慢性心血管疾病发生、发展的危险因素。
Objective To analyze the correlation between apolipoprotein E(ApoE)gene polymorphisms and the incidence rate of chronic cardiovascular disease as well as the blood lipid levels of patients.Methods ApoE gene polymorphism and lipid levels were measured by suing gene chip analysis system and biochemical analyze in 1 414 cases of chronic cardiovascular disease patients(experimental groups)and 374 cases of healthy subjects(control group).Results Compared with control group,E3/4genotype frequency was increased in experimental group,while E2/E3 genotype frequency decreased(P<0.05).Compared with control group,the levels of total cholesterol(TC),triglyceride(TG),low density lipoprotein-cholesterol(LDL-C)were obviously increased and the level of HDL-C was decreased in experimental group(P<0.05).Compared with patients with E2/E3 genotype,the level of HDL-C in patients with E3/E4 genotype was decreased and the levels of TC,LDL-C were increased significantly(P<0.05).Proportions of different ApoE genotypes in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2 diabete and fatty liver were different.Compared with the E2/E3 genotype,the proportion of the E3/E4 genotype in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2diabete and fatty liver were increased(P<0.05).Conclusion ApoE gene polymorphism might be important cause of the individual difference of lipid levels and a risk factor for the occurrence and development of chronic cardiovascular diseases.
Objective To analyze the correlation between apolipoprotein E(ApoE)gene polymorphisms and the incidence rate of chronic cardiovascular disease as well as the blood lipid levels of patients.Methods ApoE gene polymorphism and lipid levels were measured by suing gene chip analysis system and biochemical analyze in 1 414 cases of chronic cardiovascular disease patients(experimental groups)and 374 cases of healthy subjects(control group).Results Compared with control group,E3/4genotype frequency was increased in experimental group,while E2/E3 genotype frequency decreased(P<0.05).Compared with control group,the levels of total cholesterol(TC),triglyceride(TG),low density lipoprotein-cholesterol(LDL-C)were obviously increased and the level of HDL-C was decreased in experimental group(P<0.05).Compared with patients with E2/E3 genotype,the level of HDL-C in patients with E3/E4 genotype was decreased and the levels of TC,LDL-C were increased significantly(P<0.05).Proportions of different ApoE genotypes in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2 diabete and fatty liver were different.Compared with the E2/E3 genotype,the proportion of the E3/E4 genotype in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2diabete and fatty liver were increased(P<0.05).Conclusion ApoE gene polymorphism might be important cause of the individual difference of lipid levels and a risk factor for the occurrence and development of chronic cardiovascular diseases.
引文
[1]黄刚,袁刚,汪道文.载脂蛋白及其基因多态性与冠心病的关系[J].临床内科杂志,2008,25(2):143-144.
[2]Siest G,Pillot T,Regisbailly A,et al.Apolipoprotein E:an important gene and protein to follow in laboratory medicine[J].Clin Chem,1995,41(8):1068-1086.
[3]王永卿,吴婵娟,姚敏,等.黎族心脑血管疾病患者apoE基因多态性分析[J].检验医学,2012,27(4):308-310.
[4]Stengard JH,Zerba KE,Pekkanen J,et al.Apolipoprotein E polymorphism predicts death from coronary heart disease in a longitudinal study of elderly Finnish men[J].Circulation,1995,91(2):265-269.
[5]杨胜利,何秉贤,何作云,等.新疆维汉两民族冠心病患者载脂蛋白E基因的多态性[J].中国动脉硬化杂志,2003,11(5):429-434.
[6]肖志杰,赵水平,聂赛,等.载脂蛋白E基因多态性对血脂的影响[J].中华流行病学杂志,2005,26(7):533-536.
[7]Dallongeville J,Lussier-Cacan S,Davignon J.Modulation of plasma triglyceride levels by ApoE phenotype:a metaanalysis[J].J Lipid Res,1992,33(4):447-454.
[8]Dallongeville J,Tiret L,Visvikis S,et al.Effect of ApoE phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction:the EARS II study.European Atherosclerosis Research Study[J].Atherosclerosis,1999,145(2):381-388.
[9]Cullen P,Cignarella A,Brennhausen B,et al.Phenotypedependent differences in apolipoprotein E metabolism and in cholesterol homeostasis in human monocyte-derived macrophages[J].J Clin Invest,1998,101(8):1670-1677.
[2]Siest G,Pillot T,Regisbailly A,et al.Apolipoprotein E:an important gene and protein to follow in laboratory medicine[J].Clin Chem,1995,41(8):1068-1086.
[3]王永卿,吴婵娟,姚敏,等.黎族心脑血管疾病患者apoE基因多态性分析[J].检验医学,2012,27(4):308-310.
[4]Stengard JH,Zerba KE,Pekkanen J,et al.Apolipoprotein E polymorphism predicts death from coronary heart disease in a longitudinal study of elderly Finnish men[J].Circulation,1995,91(2):265-269.
[5]杨胜利,何秉贤,何作云,等.新疆维汉两民族冠心病患者载脂蛋白E基因的多态性[J].中国动脉硬化杂志,2003,11(5):429-434.
[6]肖志杰,赵水平,聂赛,等.载脂蛋白E基因多态性对血脂的影响[J].中华流行病学杂志,2005,26(7):533-536.
[7]Dallongeville J,Lussier-Cacan S,Davignon J.Modulation of plasma triglyceride levels by ApoE phenotype:a metaanalysis[J].J Lipid Res,1992,33(4):447-454.
[8]Dallongeville J,Tiret L,Visvikis S,et al.Effect of ApoE phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction:the EARS II study.European Atherosclerosis Research Study[J].Atherosclerosis,1999,145(2):381-388.
[9]Cullen P,Cignarella A,Brennhausen B,et al.Phenotypedependent differences in apolipoprotein E metabolism and in cholesterol homeostasis in human monocyte-derived macrophages[J].J Clin Invest,1998,101(8):1670-1677.