期刊文献+

慢性充血性心力衰竭患者新型趋化因子循环Fractalkine及其受体CX3CR1水平研究 被引量:18

Investigation of Circulating Fractalkine and its Receptor CX3CR1 Levels in Patients With Chronic Congestive Heart Failure
下载PDF
导出
摘要 目的:观察慢性充血性心力衰竭(CHF)患者新型趋化因子循环Fractalkine及其受体C3CXR1水平变化情况。方法:选取CHF患者(CHF组)55例和同期我院门诊健康体检者25例为正常对照组。患者入院即刻抽取静脉血,酶联免疫吸附法(ELISA)检测血清可溶性Fractalkine水平,流式细胞仪检测外周血单核细胞受体CX3CR1水平的表达;并对血清可溶性Fractalkine的水平与N末端B型利钠肽原(NT-pro BNP)水平进行相关性分析。结果:CHF组血清可溶性Fractalkine水平明显高于正常对照组(P=0.004),纽约心功能分级(NYHY)Ⅲ、Ⅳ级者明显高于Ⅱ级者;CHF组循环单个核细胞CX3CR1的表达水平较正常对照组(14.7±8.1)明显增高(P<0.05),并且随着NYHY程度加重,表达水平亦明显增高[NYHAⅡ级者为25.1±12.4,与正常对照组比(P=0.03);Ⅲ级者为37.3±11.0,与NYHAⅡ级者比(P=0.04);Ⅳ级者为41.7±11.1,与NYHAⅡ级者比(P=0.009),差异均有统计学意义]。血清可溶性Fractalkine的水平与NT-proB NP水平呈正相关(r=0.364,P<0.01)。结论:循环Fractalkine及其受体CX3CR1可能参与了慢性充血性心力衰竭患者炎症免疫发病过程。 Objective: To observe the changes of circulating fractalkine and its receptor CX3CR1 level in patients with chronic congestive heart failure(CHF).Methods: Our work included 2 group, CHF group, n=55 patients and Control group, n=25 healthy subjects. Plasma level of soluble fractalkine(sF KN) was measured by ELISA, CX3CR1 in peripheral blood mononuclear cell was examined by flow cytometry method. The relationship between sF KN and NT-proB NP was studied.Results: Compared with Control group, CHF group had increased sF KN level, P=0.004, and the patients with NYHY III, IV were more than NYHY II, and CHF group also had the higher CX3CR1 expression(14.7 ± 8.1), P0.05. The CX3CR1 level increased accordingly with NYHY classification, as the patients with NYHY II, CX3CR1 was at(25.1 ± 12.4), P=0.03 compare with Control group; with NYHY III, CX3CR1 was at(37.3 ± 11.0), P=0.04 compared with NYHY II; with NYHY IV, CX3CR1 was at(41.7 ± 11.1), P=0.009 compared with NYHY II. The circulating sF KN level was positively related to proBNP level(r=0.364, P0.01). Conclusion: The circulating FKN l and its receptor CX3CR1 might be involved in pathogenesis of immune-inflammatory pathogenesis in CHF patients.
出处 《中国循环杂志》 CSCD 北大核心 2014年第12期992-995,共4页 Chinese Circulation Journal
基金 国家自然科学基金资助项目资助(No.81470386) 高等学校博士点新教师基金资助(No.20090071120027)
关键词 FRACTALKINE 慢性充血性心力衰竭 炎症免疫 Fractalkine Chronic heart failure Immune-inflammatory
  • 相关文献

参考文献3

二级参考文献33

  • 1姚康,葛均波,孙爱军,洪晓武,施鸿毓,黄榕翀,贾庆哲,王克强,钟翠平,曹雪涛,邹云增.高糖对人单核细胞源树突状细胞分化成熟和免疫功能的影响及其机制研究[J].中华心血管病杂志,2006,34(1):60-64. 被引量:18
  • 2Molkentin JD,Lu JR,Antos CL,et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell, 1998,93:215-228.
  • 3Diedrichs H, Chi M, Boelck B, et al. Increased regulatory activity of the calcineurin/NFAT pathway in human heart failure. Eur J Heart Fail,2004,6:3-9.
  • 4Choudhary R, Sastry BK, Subramanyam C. Positive correlations between serum calcineurin activity and left ventricular hypertrophy. Int J Cardiol,2005,105:327-331.
  • 5Li J, Wang J, Russell FD, et al. Activation of calcineurin in human failing heart ventricle by endothelin-1, angiotensin Ⅱ and urotensin Ⅱ. Br J Pharmacol,2005 ,145 :432-440.
  • 6Hasenfuss G. Alterations of calcium-regulatory proteins in heart failure. Cardiovasc Res, 1998,37:279-289.
  • 7Wilkins BJ, Dai YS, Bueno OF, et al. Calcineurin/NFAT coupling participates in pathological, but not physiological, cardiac hypertrophy. Circ Res ,2004,94 : 110-118.
  • 8Taigen T, De Windt LJ, Lim HW, et al. Targeted inhibition of calcineurin prevents agonist-indueed cardiomyocyte hypertrophy. Proc Natl Acad Sci USA ,2000,97 : 1196-1201.
  • 9Grammer JB, Bleiziffer S, Monticelli F, et al. Calcineurin and matrix protein expression in cardiac hypertrophy:evidence for calcineurin B to control excessive hypertrophic signaling. Basic Res Cardiol, 2006, 101:292-300.
  • 10Romano S, Necozione S, Guarracini L, et al. Accuracy of N-terminal pro-brain natriuretic peptide in the identification of left ventricular dysfunction in high-risk asymptomatic patients. J Cardiovasc Med (Hagerstown) ,2009,10:238-244.

共引文献19

同被引文献130

引证文献18

二级引证文献135

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