期刊文献+

冠心病患者血清内脂素水平与炎症标志物及组织因子的关系 被引量:4

Relationship between serum visfatin and inflammatory markers and tissue factors in patients with coronary heart disease
下载PDF
导出
摘要 目的探讨冠状动脉粥样硬化性心脏病(冠心病)患者血清内脂素与磷酸化c-jun、CD40L及组织因子(TF)的关系。方法选择不稳定型心绞痛患者65例(UAP组)、稳定型心绞痛(SAP)患者75例、对照组60例,采用ELISA方法测定血清内脂素、磷酸化c-jun、TF及组织因子途径抑制物(TFPI)浓度水平,采用流式细胞技术测定CD40L平均荧光强度。结果 UAP组患者血清内脂素、磷酸化c-jun、CD40L、TF、TFPI水平及TF/TFPI值高于SAP组及对照组(P<0.05或P<0.01);SAP组上述指标均高于对照组(P<0.05或P<0.01)。线性相关分析显示冠心病患者血清内脂素水平与磷酸化c-jun、CD40L、TF、TFPI水平及TF/TFPI值呈正相关(P均<0.01)。多重线性逐步回归分析表明冠心病患者血清内脂素水平与磷酸化c-jun、CD40L、TF水平呈独立正相关(P均<0.01)。结论血清内脂素水平升高可能促进炎症标志物磷酸化c-jun、CD40L及组织因子生成,影响冠心病发生、发展及预后。 Objective To investigate the relationship between serum visfatin and phosphorylated c-Jun,CD40L and tissue factors (TF)in patients with coronary heart disease.Methods In total,200 sub-jects were enrolled in this study and divided into the control group(n =60),unstable(n =65)and stable angi-na groups(n =75 ).Serum visfatin,phosphorylated c-Jun,TF and tissue factor pathway inhibitor (TFPI) were measured using ELLSA,while the percentage of positive CD40L was quantified by flow cytometry.Re-sults The serum levels of visfatin,phosphorylated c-Jun,CD40L,TF,TFPI and the ratio of TF /TFPI in the stable angina group were significantly higher compared with those in the control group(P 〈0.05 or P 〈0.01 ).All these parameters in patients with unstable angina were significantly higher than their counterparts with stable angina (P 〈0.05 or P 〈0.01 ).Linear correlation analysis revealed that serum visfatin was positively correla-ted with phosphorylated c-Jun,CD40L,TF,TFPI and TF /TFPI (all P 〈0.01 ).Multiple linear stepwise re-gression analysis demonstrated that serum visfatin was independently and positively associated with phosphoryla-ted c-Jun,CD40L and TF(all P 〈0.01 ).Conclusion Hypervisfatinemia probably influences the incidence, development and prognosis of coronary heart disease by elevating the levels of phosphorylated c-Jun,CD40L and TF.
出处 《新医学》 2014年第10期652-655,共4页 Journal of New Medicine
基金 天津市卫生局科技基金资助(2010KY06)
关键词 冠状动脉粥样硬化性心脏病 内脂素 磷酸化 C-JUN CD40L 组织因子 Coronary heart disease Visfatin Phosphorylated c-Jun CD40L Tissue factor
  • 相关文献

参考文献13

  • 1Zhong M, Tan HW, Gong HP, et al. Increased serum visfatin in patients with metabolic syndrome and carotid atherosclerosis. Clin Endocrinol (Oxf), 2008, 69: 878-884.
  • 2杨丽霞,郭瑞威,齐峰,苗贵华,王先梅,石燕昆,李明秋.巨噬细胞游走抑制因子及其下游信号通路血浆水平与冠状动脉病变程度的相关性[J].中华心血管病杂志,2008,36(10):912-915. 被引量:7
  • 3Lievens D, Eijgelaar WJ, Biessen EA, et al. The multi- functionality of CIMOL and its receptor CIM0 in athero- sclerosis. Thromb Haemost, 2009, 102: 206-214.
  • 4Breitenstein A, Tanner FC, Ltischer TF. Tissue factor and cardiovascular disease : quo vadis? Circ J, 2010, 74 : 3-12.
  • 5Romacho T, S6nchez-Ferrer CF, Peir6 C. Visfatin/ Nampt: an adipokine with cardiovascular impact. Medi- ators Inflamm, 2013: 946427.
  • 6Liu SW, Qiao SB, Yuan JS, et al. Visfatin stimulates production of monocyte chemotactic protein-1 and inter- leukin-6 in human vein umbilical endothelial cells. Horm Metab Res, 2009, 41: 281-286.
  • 7Lee WJ, Wu CS, Lin H, et al. Visfatin-induced expres- sion of inflammatory mediators in human endothelial cells through the NF-kappaB pathway. Int J Obes (Lond), 2009, 33: 465-472.
  • 8Oita RC, Ferdinando D, Wilson S, et al. Visfatin in- duces oxidative stress in differentiated C2C12 myotubes in an Akt- and MAPK-independent, NFkB- dependent manner. Pflugers Arch, 2010, 459: 619-630.
  • 9Huang Q, Guo Y, Zeng H, et al. Visfatin stimulates a cellular renin-angiotensin system in cultured rat mesang- ial ceils. Endoer Res, 2011, 36: 93-100.
  • 10Ding G, Zhang A, Huang S, et al. ANG Ⅱ induces c- Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR. Am J Physiol Renal Physiol, 2007, 293 : F1889-F1897.

二级参考文献14

  • 1Hsiang CY, Wu SL, Chen JC, et al. Acetaldehyde induces matrix metalloproteinase-9 gene expression via nuclear factor-kappaB and activator protein 1 signaling pathways in human hepatocellular carcinoma cells: association with the invasive potential. Toxicol Lett, 2007,171:78-86.
  • 2Onodera S, Nishihira J, Iwabuchi K, et al. Macrophage migration inhibitory factor up-regulates matrix metalloproteinase-9 and -13 in rat osteoblasts. Relevance to intracellular signaling pathways. J Biol Chem, 2002, 277:7865-7874.
  • 3Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol, 1983, 51:606.
  • 4ACC/AHA Task Force. Guidelines for percutaneous transluminal coronary angioplasty. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures ( Subcommittee on Percutaneous Transluminal Coronary Angioplasty). J Am Coll Cardiol, 1988, 12:529-545.
  • 5Surh Y J, Na HK, Lee SS. Transcription factors and mitogenactivated protein kinases as molecular targets for chemoprevention with anti-inflammatory phytochemicals. Biofactors, 2004,21 : 103- 108.
  • 6Dagnell C, Kemi C, Klominek J, et al. Effects of neurotrophins on human bronchial smooth muscle cell migration and matrix metalloproteinase-9 secretion. Transl Res, 2007,150:303-310.
  • 7Luttun A, Lutgens E, Manderveld A, et al. Loss of Matrix metalloproteinase-9 or Matrix metalloproteinase-12 protects apolipoprotein E-deficient mice against atherosclerotic aedia destruction but differentially affects plaque growth, Circulation, 2004,109 : 1408-1414.
  • 8Zeng B, Prasan A, Fung KC, et al. Elevated circulating levels of matrix metalloproteinase-9 and -2 in patients with symptomatic coronary artery disease. Intern Med J, 2005,35:331-335.
  • 9Verna L, Ganda C, Stemerman MB. In vivo low-density lipoprotein exposure induces intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 correlated with activator protein-1 expression. Arterioscler Thromb Vasc Biol, 2006,26 : 1344-1349.
  • 10Chandrasekar B, Mummidi S, Mahimainathan L, et al. Interleukin-18-induced human coronary artery smooth muscle cell migration is dependent on NF-kappaB- and AP-1-mediated matrix metalloproteinase-9 expression and is inhibited by atorvastatin. J Biol Chem. 2006,281:15099-15109.

共引文献6

同被引文献37

引证文献4

二级引证文献10

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