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冠心病患者细胞因子信号转导抑制剂1基因多态性的临床意义 被引量:6

Clinical Significance of SOCS1 Gene Polymorphism in Patients with Coronary Heart Disease
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摘要 目的探讨冠心病患者细胞因子信号转导抑制剂1(SOCS1)基因多态性与心功能及细胞因子的相关性。方法选择冠心病患者256例为研究组,健康自愿者256例为对照组。运用聚合酶链反应(PCR)及单核苷酸多态性(SNP)技术分析2组SOCS1基因多态性,并测定细胞因子和心功能的变化。结果 2组SOCS1基因rs173516427和rs15677380等位基因频率差异有统计学意义(χ2=7.46、8.09,P=0.024、0.014),rs173516427 G等位基因和rs15677380 C等位基因为冠心病的高危因素(OR=1.56、1.71);rs15677380、rs173516427不同基因型LVEF和BNP差异有统计学意义(F=10.9、12.3、9.89、11.5,P<0.05)。结论SOCS1基因与动脉粥样硬化的发生有关,并参与冠心病的发展过程。 Objective To explore the relationship between SOCS1 gene polymorphism and heart function and cellular factors in patients with coronary heart disease. Methods A total of 256 patients with coronary heart disease were included for the study group and 256 normal people were selected as the control group. The polymorphism of SOCSI gene were determined by polymerase chain reaction and single nucleotide polymorphism. The heart function and cellular factors were detected. Results The difference of the rs173516427 and rs15677380 'allele frequencies between the study group and the control group was significantly (X2=7.46,8.09,P =0.024,0.014). The G al- lele of rs173516427 and C allele of the rs15677380 were risk factors to coronary heart disease (OR=1.56, 1.71 );the difference of LVEF and BNP among the rs15677380 and rs173516427 genotype was significantly (F =10.9,12.3,9.89, 11.5,P 〈 0.05). Conclusion There is an correlation between the SOCS1 gene polymorphism and carotid atherosclemsis. The SOCSI gene participates in the development of coronary heart disease.
出处 《中国医科大学学报》 CAS CSCD 北大核心 2013年第5期436-438,450,共4页 Journal of China Medical University
基金 河南省科技厅科研计划(092102310203)
关键词 动脉粥样硬化 细胞因子信号转导抑制剂1基因 多态性 carotid atherosclerosis SOCSI gene polymorphism
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  • 1Ridker PM, Hennekens CH, Stampfer MJ. Plasma concentration of soluble intercellular adhesion moleculel and risks of future myocardial infarction in apparently healthy men [J ]. Lancet, 1998, 351(1): 88.
  • 2Yanagisawa M. A Novel potent vasoconstrictor peptide produced by vascula rendcthetial cells[J]. Nature, 1988, 332(5): 411.
  • 3Sudoh T, Minamino N, Kangwa K, et al. A new natriuretic peptide in human brain [ J ]. Nature, 1988, 322(5): 78-81.
  • 4Danesh J, Whincup P, Walker M, et al. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses[J]. BMJ, 2000, 321(7255): 199.
  • 5Groenning B A, Nilsson J C, Sondergaard L, et al. Evaluation of impaired left ventricular ejection fraction and increased dimensions bymultiple neurohumoral plasma concentrations [J]. Eur J Heart Fail, 2001,3(6) :699-708.
  • 6Tao L, Gao E, Jiao X, et al. Adiponectin cardiopmteetion after myocardial ischemia-reperfusion involves the reduction of oxidative/nitrativestress[J]. Circulation, 2007,115 ( 11 ) : 1408- 1416.
  • 7De Silva R, Nikitin N P, Witte K K, et al. Incidence of renal dysfunction over 6 ITlonths in patients wi th chronic heart failure due to left ventrieular systolic dysfunction: contributing factors and relationship to Prognosis [J]. Eur Heart J, 2006,27(5) :569-581.
  • 8Yamada T, Node K, Mine T, et al. Long-term effect of atorvastatin on neurohumoral activation and cardiac function in patients with chronic heart failure: a prospective randomized controlled study [J]. Am Heart J, 2007,153(6): 1055,e1-e8.
  • 9Arima H, Kubo M, Yonemoto K, et al. High sensitivity C- reactive protein and coronary heart disease in a general populationof Japanese:the Hisayama study [J]. Arterioscler Thromb Vasc Biol, 2008,28(7) : 1385-1391.
  • 10叶任高,陆再英.内科学[M].6版.北京:人民卫生出版社,2005.948-987.

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  • 1殷惠军,王显刚,史大卓.蒺藜总皂苷对心肌缺血再灌注损伤炎症因子TNF-α、IL-1β释放的影响[J].解放军医学杂志,2006,31(10):986-987. 被引量:16
  • 2Ross R. Atherosclerosis-an inflammatory disease [ J ]. N Engl J Med,1999,340(2) : 115-126.
  • 3Tu Y. The discovery of artemisinin (qinghaosu) and gifts from Chi- nese medicine[J]. Nat Med,2011,17(10) : 1217-1220.
  • 4Lai HC, Singh NP, Sasaki T. Development of artemisinin compounds for cancer treatment [ J ]. Invest New Drugs, 2013,31 ( 1 ) : 230-246.
  • 5Park KH, Yoon YD, Han SB, et al. Artemisinin inhibits lipopolysae- charide-induced interferon-beta production in RAW 264.7 cells : im- plications on signal transducer and activator of transcription- 1 sig- naling and nitric oxide production[J:. Int Immunopharmacol, 2012, 14(4) :580-584.
  • 6Galkina E, Ley K. hnmune and inflammatory mechanisms of athero- sclerosis [ J ]. Annu Rev Immunol, 2009,1 (27) : 165-197.
  • 7Goetze S, Kiutseher U, Kaneshiro K, et al. TNF-alpha induces ex- pression of transcription factors c-fos, Egr- 1, and Ets- 1 in vascular lesions through extracellular signal-regulated kinases 1/2 [Jl. Ath- erosclerosis, 2001,159 ( 1 ) : 93 - 101.
  • 8Tsuji T, Miyazaki M, Sakaguchi M, et al. A REIC gene shows down- regulation in human immortalized cells and human tumor-derived cell lines [J 1. Biochem Biophys Res Commun, 2000,268 ( 1 ) : 20-24.
  • 9Wang Z, Hu W, Zhang JL, et al. Dihydroartemisinin induces autoph- agy and inhibits the growth of iron-loaded human myeloid leukemia K562 cells via ROS toxicity [Jl. FEBS Open Biol, 2012, 23 (2) : 103-112.
  • 10Barseghian A, Gawande D, Bajaj M. Adiponectin and vul- nerable atherosclerotic plaques [J]. J Am Coll Cardiol,2011, 57(7) :761-770.

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