>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
APOE基因多态性及其与环境因素的交互作用对颈动脉粥样硬化的影响
作者:桂玉琪1  郭怡菁1 2  刘瑷瑜1  田秀秀1  郭晓颖1  吴珊珊1 
单位:1. 东南大学 医学院, 江苏 南京 210009;
2. 东南大学附属中大医院 神经内科, 江苏 南京 210009
关键词:APOE基因多态性 颈动脉粥样硬化 环境因素 交互作用 
分类号:R543.5
出版年·卷·期(页码):2020·39·第二期(175-180)
摘要:

目的:研究APOE基因多态性是否会影响颈动脉粥样硬化(CAS)的发病风险,以及APOE基因多态性与环境因素的交互作用对CAS发病风险的可能影响,以期为CAS的预防和治疗提供新的方向和个体化的方案。方法:入组332例(筛除ε2/4型),行Hardy-Weinberg检验,验证入组研究对象的基因型分布是否具有代表性。通过二元Logistic回归分析检验APOE基因多态性及其与环境因素的交互作用对CAS存在性的影响。结果:总样本人群的基因分布有代表性。E2、E3和E4组临床资料无明显差异。在总样本中,APOE基因多态性与CAS的发病风险无明显相关(P>0.05)。而按年龄和吸烟史分层分析后,在不吸烟男性中,校正血脂前后E2型的CAS发病风险均明显低于E3型(P=0.007,P=0.004),校正血脂前后E4型与E3型相比发病风险无明显差异(P=0.999)。在不吸烟女性和吸烟男性中,校正血脂前后均未发现APOE基因多态性对CAS发病风险的影响(P>0.05)。结论:在总人群中,APOE基因多态性与CAS发病风险无明显相关。不吸烟人群中,较之ε3,ε2对男性CAS的发病有保护作用而对女性无保护作用。在男性中,较之ε3,ε2对不吸烟者有保护作用而对吸烟者该保护作用不显著。

Objective: To investigate the effect of APOE gene polymorphism and its interaction with environmental factors on the risk of carotid atherosclerosis(CAS), and to provide new directions and an individualized therapeutic approach for the prevention and treatment of CAS. Methods: Three hundred and thirty-two subjects (exclucingε2/4 genotype) were enrolled in this study. Hardy-Weinberg principle was employed to test the representativeness of subjects' genotype distribution. The effects of APOE gene polymorphism and its interaction with environmental factors on the risk of CAS were examined by binary logistic regression analysis. Results: The representativeness of genotype distribution of the subjects was confirmed. Clinical data of E2, E3 and E4 groups did not show significant differences. Among all subjects, APOE gene polymorphism was not significantly associated with the risk of CAS (P>0.05). After stratifying all subjects by age and smoking history, the risk of CAS in E2 group was significantly lower than that in E3 group(P=0.007, P=0.004) in male non-smokers before and after adjusting the blood lipid levels, while there was no significant difference in the risk of CAS between E4 and E3 groups(P=0.999). Among non-smoking women and smoking men, the effect of APOE gene polymorphism on the risk of CAS was not found before and after adjusting blood lipid levels(P>0.05). Conclusion: APOE gene polymorphism does not have significant influence on the risk of CAS. Among non-smokers, ε2 has a protective effect upon the risk of CAS in males but not in females as compared with ε3. In males,ε2 has a protective effect on the risk of CAS in non-smokers compared with ε3, but the effect is not significant in smokers.

参考文献:

[1] ZHAO X,LI R,HIPPE D S,et al.Chinese Atherosclerosis Risk Evaluation(CARE Ⅱ) study:a novel cross-sectional,multicentre study of the prevalence of high-risk atherosclerotic carotid plaque in Chinese patients with ischaemic cerebrovascular events-design and rationale[J].Stroke Vasc Neurol,2017,2(1):15-20.
[2] KOFLER B M,MILES E A,CURTIS P,et al.Apolipoprotein E genotype and the cardiovascular disease risk phenotype:impact of sex and adiposity(the FINGEN study)[J].Atherosclerosis,2012,221(2):467-470.
[3] HUMPHRIES S E,TALMUD P J,HAWE E,et al.Apolipoprotein E4 and coronary heart disease in middle-aged men who smoke:a prospective study[J].Lancet,2001,358(9276):115-119.
[4] ZHANG Z,CHEN X,BAUM L,et al.Association between the apolipoprotein E gene polymorphism and atherosclerotic middle cerebral artery stenosis[J].Neurologist,2018,23(2):47-50.
[5] HATTERS D M,PETERS-LIBEU C A,WEISGRABER K H.Apolipoprotein E structure:insights into function[J].Trends Biochem Sci,2006,31(8):445-454.
[6] JOFRE-MONSENY L,MINIHANE A M,RIMBACH G.Impact of apoE genotype on oxidative stress,inflammation and disease risk[J].Mol Nutr Food Res,2008,52(1):131-145.
[7] MASTROIANNO S,DI STOLFO G,SERIPA D,et al.Role of the APOE polymorphism in carotid and lower limb revascularization:a prospective study from Southern Italy[J].PLoS One,2017,12(3):e171055.
[8] ZURNIC I,DJURIC T,KONCAR I,et al.Apolipoprotein E gene polymorphisms as risk factors for carotid atherosclerosis[J].Vojnosanit Pregl,2014,71(4):362-367.
[9] YOUSUF F A,IQBAL M P.Apolipoprotein E(ApoE) gene polymorphism and coronary heart disease in Asian populations[J].Pak J Pharm Sci,2015,28(4):1439-1444.
[10] BLAZEJEWSKA-HYZOREK B,GROMADZKA G,SKOWRONSKA M,et al.APOE epsilon 2 allele is an independent risk factor for vulnerable carotid plaque in ischemic stroke patients[J].Neuro Res,2014,36(11):950-954.
[11] TALMUD P J,STEPHENS J W,HAWE E,et al.The significant increase in cardiovascular disease risk in APOE epsilon 4 carriers is evident only in men who smoke:potential relationship between reduced antioxidant status and ApoE4[J].Ann Hum Genet,2005,69(Pt 6):613-622.
[12] SEIP R L,ZOELLER R F,ANGELOPOULOS T J,et al.Interactive effects of APOE haplotype,sex,and exercise on postheparin plasma lipase activities[J].J Appl Physiol,2011,110(4):1021-1028.
[13] KIM J A,CHUN E J,LEE M S,et al.Relationship between amount of cigarette smoking and coronary atherosclerosis on coronary CTA in asymptomatic individuals[J].Int J Cardiovasc Imaging,2013,29(1):21-28.
[14] KOHASHI K,NAKAGOMI A,MORISAWA T,et al.Effect of smoking status on monocyte tissue factor activity,carotid atherosclerosis and long-term prognosis in metabolic syndrome[J].Circ J,2018,82(5):1418-1427.
[15] SHAH P K.Inflammation,infection and atherosclerosis[J].Trends Cardiovasc Med,2019,29(8):468-472.
[16] POLEDNE R,LESA I K.Inflammation and atherosclerosis[J].Vnitr Lek,2019,64(12):1142-1146.
[17] ATTARD R,DINGLI P,DOGGEN C,et al.The impact of passive and active smoking on inflammation,lipid profile and the risk of myocardial infarction[J].Open Heart,2017,4(2):e620.
[18] KIANOUSH S,YAKOOB M Y,AL-RIFAI M,et al.Associations of cigarette smoking with subclinical inflammation and atherosclerosis:ELSA-Brasil(the brazilian longitudinal study of adult health)[J].J Am Heart Assoc,2017,6(6):e005088.
[19] MCEVOY J W,NASIR K,DEFILIPPIS A P,et al.Relationship of cigarette smoking with inflammation and subclinical vascular disease:the multi-ethnic study of atherosclerosis[J].Arterioscler Thromb Vasc Biol,2015,35(4):1002-1010.
[20] 张东平,张波,胡长林.ApoE基因多态性与颈动脉粥样硬化斑块稳定性的相关性研究[J].重庆医科大学学报,2015,40(1):78-82.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 233105 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-87232481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364