期刊文献+

外周血单核细胞TLR-4在冠心病合并糖尿病中的表达及其意义

Relationship between TLR4 on PBMC and diabetic mellitus in coronary heart disease patients
暂未订购
导出
摘要 目的 探讨外周血单核细胞(PBMC)Toll样受体4(TLR4)在冠心病合并糖尿病中的表达及其意义.方法 分组:健康对照组40例,糖尿病组36例,冠心病组43例,冠心病合并糖尿病组40例.采用SYBR Green Ⅰ实时荧光定量RT-PCR和流式细胞仪检测PBMC TLR-4的表达.结果 与对照组相比,糖尿病、冠心病及冠心病合并糖尿病组的TLR4 mRNA表达水平和TLR4阳性细胞百分比均上调(均P<0.05);糖尿病与冠心病两组间差异无统计学意义,而冠心病合并糖尿病组显著高于糖尿病组和冠心病组(均P<0.05).Logistic回归分析显示,TLR-4是冠心病并发糖尿病的危险因素(OR =4.048,P<0.01).结论 TLR4在糖尿病合并冠心病共同的发病基础中可能起着一定作用. Objective To study the Relationship between Toll-like receptor 4(TLR4)in Peripheral-blood mononuclear cells(PBMC) and diabetic me]litus(DM) in coronary heart disease(CHD) patients. Methods Control group(n=40), DM group (rt=36), CHD group (n=43) and CHD wih DM group (n=40). The expressions of TLR4 mR- NA and TLR4 protein on PBMC were examined by SYBR Green I real-time quantitative reverse transcription ploymerse chain reaction (RT-PCR) and Flow cytometric analysis respectively. Results compared with control group, the expressions of TLR4 mRNA and TLR4 protein were upgraded in DM group,CHD group and CHD wih DM group,and difference was no statistically significant between DM group and CHD group. Compared with DM group and CHD group, the level of TLR4 increased in CHD wih DM group (P〈0.05). Logistic regression analysis showed that TLR-4 is the risk factor in the progression of DM in CHD(OR=4.048, P〈O.O1). Conclusion TLR-4 may play a minor role in the the common oathogenetic basis of CHD wih DM.
出处 《中国心血管病研究》 CAS 2013年第10期775-778,共4页 Chinese Journal of Cardiovascular Research
关键词 冠心病 糖尿病 外周血单核细胞 TOLL样受体4 Coronary heart disease Diabetes mellitus Peripheral-blood mononuelear cells Toll-like Receptor4
  • 相关文献

参考文献12

  • 1King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Di- abetes Care, 1998,21:1414-1431.
  • 2Bartnik M, Malmberg K, Hamsten A,et al. Abnormal glucose tol- erance--a common risk factor in patients with acute myocardial infarction in comparison with population-based controls. J Intern Med, 2004,256:288-297.
  • 3Akashi-Takamura S, Miyake K. Toll-like receptors (TLRs) and mmune disorders. J Infect Chemother. 2006, 12: 233-240.
  • 4李志强,郑兴.炎症与冠心病[J].中国心血管病研究,2006,4(3):233-235. 被引量:38
  • 5Miehelsen KS,Wong MH, Shah PK. Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces athemsclemsis and alters plaque phenotype in mice deficient in apolipoprctein E. PNAS, 2004,101:10679-10684.
  • 6Heiko Methe,Jong-Oh Kim, Sieglinde Kofler, et al. Expansion of circulating Ton-like receptor 4-positive monoeytes in patients with acute coronary syndrome. Circulation, 2005,111:2654-2661.
  • 7Xu XH,Shah PK,Faure E. Toll like receptor4 is expressedby macrophages in routine and human lipid rich at herosclemtic plaques and up regulated by oxidized LDL. Circulation,2001, 104: 3103-3108.
  • 8Miller YI,Viriyakosol S,Binder CJ,et al. Minimally modifiedLDL binds to CD14, induces macrophage spreading via TLR4/ MD 2, and inhibit s phagocytosis of apoptotic cells. J Biol Chem, 2003,278: 1561-1568.
  • 9Reyna SM, Ghosh S, Tantiwong P, et al. Elevated toll-like recep- tor 4 expression and signaling in muscle from insulin-resistant subjects. Diabetes, 2008,57:2595-2602.
  • 10吴铿,游琼,莫海亮,黄瑞娜.糖尿病心肌病外周血单核细胞Toll样受体4、肿瘤坏死因子-α的表达及其与心肌灌注的相关性[J].中华心血管病杂志,2011,39(6):503-507. 被引量:7

二级参考文献54

  • 1[1]Reaven G. Metabolic syndrome. Pathophysiology and implications for the management of cardiovascular disease[J]. Circulation, 2002(106): 186 - 188
  • 2[3]Cleeman JI. Executive summary of the third report of the national cholesterol education program(NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. (adults treatment Panel Ⅲ) [J]. JAMA, 2001,285: 2486 - 2497
  • 3[1]Ross R.Atherosclerosis-an inflammation disease.N Engl Med,1999,340:115-126.
  • 4[2]Massberg S,Brand K,Gruner S,et al.A critical role of platelet adhesion in the initiation of atherosclerotic lesion formation.Exp Med,2002,196:887-896.
  • 5[3]Boring L,Gosling J,Cleary M,et al.Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis.Nature,1998,394:894 -897.
  • 6[4]Gupta S,Pablo AM,Jiang X,et al.IFN-gamma potentiates atherosclerosis in apoE knock-out mice.Clin Invest,1997,99:2752-2761.
  • 7[5]Mallat Z,Corbaz A,Scoazec A,et al.Interleukin- 18/interleukin-18 binding protein signaling modulates atherosclerotic lesion development and stability.Circ Res,2001,89:E41-E45.
  • 8[6]Ludewig B,Freigang S,Jaggi M,et al.Linking immunemediated arterial inflammation and cholesterol-induced atherosclerosis in a transgenic mouse model.Proc Natl Acad Sci USA,2000,97:12752-12757.
  • 9[7]Robertson AKL,Rudling M,Zhou X,et al.Disruption of TGF-beta signaling in T cells accelerates atherosclerosis.J Clin Invest,2003,112:1342- 1350.
  • 10[8]Binder C J,Hrkk S,Dewan A,et al.Pneumococcal vaccination decreases atherosclerotic lesion formation:molecular mimicry between Streptococcus pneumoniae and oxidized LDL.Nat Med,2003,9:736-743.

共引文献55

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部