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白介素10基因-592A/C多态性与颈动脉粥样硬化的关系
引用本文:谢高强,赵连成,李莹,王浩,梁立荣,史平,任福秀,武阳丰. 白介素10基因-592A/C多态性与颈动脉粥样硬化的关系[J]. 中国分子心脏病学杂志, 2008, 8(5): 305-309
作者姓名:谢高强  赵连成  李莹  王浩  梁立荣  史平  任福秀  武阳丰
作者单位:1. 中国医学科学院,阜外心血管病医院,卫生部心血管病防治研究中心
2. 北京市石景山区疾病预防控制中心
3. 中国医学科学院,阜外心血管病医院,卫生部心血管病防治研究中心;北京大学医学部公共卫生学院;乔治(中国)中心
基金项目:国家自然科学基金,国家科技攻关计划,阜外心血管病医院院所青年科学基金
摘    要:目的研究白介素10基因-592A/C多态性与颈动脉斑块的关系及吸烟-基因的交互作用。方法2005年,在北京社区整群随机抽样人群中进行流行病学调查,询问病史及吸烟等生活方式相关危险因素,检测颈动脉内中膜厚度(IMT)、颈动脉斑块、白介素10基因启动子区域-592A/C位点基因型及相关生化指标。结果共1296例无心肌梗死和脑卒中病史者进行分析,-592A/A、-592A/C和-592C/C基因型频率分别为41.9%、46.5%和11.7%,符合Hardy—Weinberg平衡(P=0.417)。单因素、多因素及分层分析发现-592A/C与作为连续变量的IMT及作为分类变量的IMT增厚均无显著相关关系。单因素分析显示,-592A/C在显性、共显性和隐性模型中与颈动脉斑块患病率均无显著性,但调整年龄和性别后,-592C/C基因型在隐性模型中对颈动脉斑块起显著保护作用(OR=0.7,95%可信限:0.45-0.98),分层分析发现吸烟与-592A/C对斑块危险存在显著交互作用(P=0.048),-592C/C的保护作用仅出现在从未吸烟人群中(OR,0.5,95%可信区间:0.3-0.8),戒烟及现吸烟人群中关联未达到统计学显著性水平。结论白介素10基因-592C/C基因型对动脉粥样硬化起到保护作用,而且这种保护作用与吸烟状况之间存在交互作用。

关 键 词:-592A/C  白介素10  颈动脉斑块  吸烟  交互作用

The Relationship Between Interleukin-10 Gene -592A/C Polymorphism and Carotid Atherosclerosis
XIE Gao-qiang,ZHAO Lian-cheng,LI Ying,WANG Hao,LIANG Li-rong,SHI Ping,REN Fu-xiu,WU Yang-feng. The Relationship Between Interleukin-10 Gene -592A/C Polymorphism and Carotid Atherosclerosis[J]. Molecular Cardiology of China, 2008, 8(5): 305-309
Authors:XIE Gao-qiang  ZHAO Lian-cheng  LI Ying  WANG Hao  LIANG Li-rong  SHI Ping  REN Fu-xiu  WU Yang-feng
Affiliation:XIE Gao-qiang, ZHAO Lian-cheng, LI Ying, WANG Hao, LIANG Li-rong, SHI Ping, REN Fu-xiu, WU Yang-feng. Division for CVD Prevention and Control Network( Xie ,Zhao ,Li,and Liang) and Division for Ul- trasound(Wang) of Cardiovascular Institute and Fuwai Hospital, CAMS & PUMC;Shijingshan CDC of Bei- ring (Shi and Ren ) ;Department of Epidemiology and Biostatistics, Peking University School of Public Health, Beijing , China( Wu ) ; The George Institute, China, Belting, China( Wu ).
Abstract:Objective To study the association between -592A/C polymorphisms in interleukin-10 (IL-10) gene and carotid plaque and smoking-gene interaction. Methods A community-based epidemiology survey was carried out in 1296 participants free of myocardial infarction and stroke in Beijing in 2005. Data on history of cardiovascular diseases and living habits, such as smoking status, were collected. Carotid IMT, plaque, and IL-10 gene polymorphisms (-592A/C) along with other anthropometric and physiologica/ were measured. Results The respective frequencies of wild-type ( - 592A/A ), heterozygous ( - 592A/C), and variant genotype ( - 592C/C) were 41.9%, 46.5%, and 11.7%, which was consistent with Hardy-Weinberg equilibrium ( P = 0. 417 ). Univariable, multivariable, and subgroups analysis found -592A/C polymorphism was not significandy associated with IMT as a continuous variable and increased IMT as a categorical variable. Univariable analysis found -592A/C polymorphism was not significantly associated with carotid plaque by dominant, semi-dominant, and recessive models. But muhivariable analysis found - 592C/C genotype was significantly associated with decreased risk of carotid plaque byrecessive model ( OR 0.7,95% CI : 0.45 - 0.98 ). Gene-risk factor interaction analyses showed that the association was significantly modified by smoking status ( P = 0.048 ). The protective effects of - 592C/C on carotid plaque by recessive model only remained significance in never smokers (OR, 0.5, 95% CI: 0.3 0.8), but not in ex-smokers and current smokers. Conclusion IL10 gene -592G/C genotype plays an important protective role on early atherosclerosis via a recessive inheritance model, which is counter-balanced by cigarette smoking.
Keywords:-592A/C  interleukin-10  Carotid plaque  Smoking  Interaction
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