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急性心肌梗死后心衰大鼠核因子-κB与炎性细胞因子的相关性研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第3期
页码:
309-312
栏目:
基础研究
出版日期:
2011-05-12

文章信息/Info

Title:
Relationship between serum nuclear factor-κB and serum inflammatory cytokines levels in heart failure following acute myocardial infarction in rats
作者:
卢琳1贾如意2
1.山东省医学科学院基础医学研究所,山东 济南 250300;2.济南市第四人民医院、济南市心血管病研究所,山东 济南 250031
Author(s):
LU Lin1 JIA Ru-yi2
1.Institute of Basic Medicine, Shandong Academy of Medical Science, Jinan 250300, Shandong, China; 2.Jinan Fourth People's Hospital, Jinan Institute of Cardiovascular Diseases, Jinan 250014, Shandong, China
关键词:
急性心肌梗死核因子-κB心力衰竭炎性细胞因子大鼠
Keywords:
nuclear factor-κB tumor necrosis factor-α high-sensitivity C-reactive protein heart failure
分类号:
R542.22
DOI:
-
文献标识码:
A
摘要:
目的:探讨急性心肌梗死后(AMI)心衰(HF)大鼠血清核因子-κB(NF-κB)的水平与肿瘤坏死因子-α(TNF-α)、高敏C反应蛋白(hsCRP)分泌的相关性。方法: 将50只SD大鼠随机分为3组:HF组(20只)、治疗组(20只)和假手术组(10只)。结扎大鼠冠状动脉前降支建立AMI后HF模型。治疗组在手术结扎后饮水中给予NF-κB抑制剂吡咯烷二硫代氨基甲酸盐(pyrrolidine dithiocarbamate,PDTC),HF组和假手术组给予同等量的蒸馏水。术后6周,行血流动力学检测;秤取心脏组织的湿质量;取动脉血分离血清,用ELISA法检测NF-κB、TNF-α的水平,用乳胶增强透射免疫比浊法检测hsCRP水平。结果: ①HF组和治疗组大鼠心室重构指数和肺指数明显高于假手术组(P<0.05)。②HF组和治疗组大鼠血流动力学的状况较假手术组明显下降(P<0.05),但治疗组较HF组有所好转(P<0.05)。③HF组和治疗组血清NF-κB、TNF-α和hsCRP的水平较假手术组明显升高(P<0.05);治疗组又较HF组明显下降(P<0.05)。④NF-κB的水平与TNF-α、hsCRP的水平呈显著的正相关(r分别为0.465和0.323,均P<0.05)。结论: AMI后HF大鼠血清NF-κB的水平升高,炎性细胞因子TNF-α和hsCRP分泌增多,HF大鼠可能是通过NF-κB水平的升高上调炎性细胞因子的分泌。
Abstract:
AIM:To study the relationship of serum nuclear factor-κB (NF-κB) and the level of serum TNF-α and high-sensitivity C-reactive protein (hsCRP) in heart failure following acute myocardial infarction (MI) in rats. METHODS: A total of 50 SD rats were randomized into three groups: heart failure group (n=20), treatment group (n=20) and sham-operated group (n=10). Heart failure model was created in rats by coronary artery ligation after MI. After ligation, NF-κB inhibitor pyrrolidine dithiocarbamate was given in drinking water in treatment group and the same amount of distilled water was given in heart failure group and sham-operated group. All surviving models were sacrificed after 6 weeks. Hemodynamic parameters and ventricular mass index were measured. Serum NF-κB and TNF-α levels were detected using ELISA and hsCRP was detected using latex-enhanced immunoturbidimetric assay transmission. RESULTS: Compared with sham-operated group, ventricular remodeling index and lung index in heart failure group and treatment group significantly increased (P<0.05). Compared with heart failure group, indexes in treatment group decreased but were still significantly higher than in sham-operated group (P<0.05). Hemodynamic status significantly decreased in heart failure group and treatment group compared with sham-operated group (P<0.05) and status in the treatment group was superior to that in the heart failure group (P<0.05). Serum NF-κB, TNF-α and hsCRP levels in heart failure group and treatment group significantly increased compared with sham-operated group (P<0.05). Levels in treatment group significantly decreased compared with heart failure group (P<0.05). NF-κB levels were positively correlated with levels of TNF-α (r=0.465, P<0.05) and levels of hsCRP (r=0.323, P<0.05). CONCLUSION: Levels of serum NF-κB and serum TNF-α and hsCRP in heart failure following acute MI in rats increased, suggesting that NF-κB upregulates the levels of inflammatory cytokines in heart failure rats.

参考文献/References

[1]Yndestad A,Damas JK,Qie E,et al.Role of inflammation in the progression of heart failure[J].Curr Cardiol Rep,2007,9(3):236-241.
[2]Braunwald E.心脏病学[M].陈灏珠,译.北京:人民卫生出版社, 2001:407-426.
[3]Bozkurt B,Kribbs SB,Clubb FJ,et al.Pathophysiologically relevent concentrations of tumor necrosis factor-α promote progressive left ventricular dysfunction and remodeling in rats[J].Circulation,1998,97(14):1382-1391.
[4]Parish RC,Evans JD.Inflammation in chronic heart failure[J].Ann Pharmacother,2008,42(7):1002-1161.
[5]Candia AM,Villacorta H Jr,Mesquita ET.Immune-inflammatory activation in heart failure[J].Arq BrasCardiol,2007,89(3):183-90,201-208.
[6]Dunlay SM,Weston SA,Redfield MM,et al.Tumor necrosis factor-alpha and mortality in heart failure: a community study[J].Circulation,2008,118(6):625-631.
[7]Liao YH,Cheng X.Autoimmunity in myocardial infarction[J].Int J Cardiol,2006,112(1):21-26.
[8]Nian M,Lee P,Khaper N,et al.Inflammatory cytokines and postmyocardial infarction remodeling[J].Circ Res,2004,94(12):1543-1553.
[9]Lu L,Chen SS,Zhang JQ,et al.Activation of nuclear factor-κB and its proinflammatory mediator cascade in the infarcted rat heart[J].Biochem Biophys Res Commun,2004,321(4):879-885.
[10]Kempe S,Kestler H,Lasar A,et al.NF-κB controls the global pro-inflammatory response in endothelial cells: evidence for the regulation of a pro-atherogenic program[J].Nucleic Acids Res.2005.33(16):5308-5319.
[11]Wang HR,Li JJ,Huang CX, et al.Fluvastatin inhibits the expression of tumor necrosis factor-alpha and activation of nuclear factor-kappaB in human endothelial cells stimulated by C-reactive protein[J].Clin Chim Acta.2005, 353(1-2):53-60.

备注/Memo

备注/Memo:
收稿日期:2010-07-30.基金项目:济南市科学技术发展计划项目[济科计字(200905036),济科合字(2009) 05052] 通讯作者:贾如意,主任医师,主要从事冠心病临床和基础研究Email:jrycardiology@sohu.com 作者简介:卢琳,硕士生Email:waitinglin99@163.com
更新日期/Last Update: 2011-03-17