外周血Toll样受体4及TNF-α与冠状动脉支架置入术后再狭窄的关系被引量：7

The relationship of peripheral blood toll like receptor 4 and TNF-α with coronary in-stent restenosis

在线阅读下载PDF

导出

摘要目的：支架术后再狭窄（in-stent restenosis,ISR）是影响冠状动脉介入疗效的主要问题,本研究探讨外周血Toll样受体4（toll like receptor4,TLR4）及TNF-α与冠状动脉支架置入术后再狭窄的相关性。方法：入选135例稳定型心绞痛患者,冠状动脉造影示单支血管病变,并成功置入支架,术后6-12个月复查冠状动脉造影,将患者分为支架术后再狭窄组和无再狭窄组,采用流式细胞技术测定支架置入术前及术后5-7d外周血单核细胞TLR4的表达量,同时用酶联免疫吸附试验法（ELISA）检测血清中TNF-α的浓度。结果：复查冠状动脉造影发现14例患者发生支架内再狭窄,占10.4%,无再狭窄组121例,占89.6%。组间比较：术前TLR4及TNF-α的表达水平在两组间差异无统计学意义。分别为：TLR4[（144.20±52.99）vs.（117.40±61.9）,P〉0.05],TNF-α[（34.32±11.97）vs.（27.47±14.47）ng/L;P〉0.05];术后5-7d两组患者TLR4与TNF-α表达均升高,且再狭窄组升高更明显：TLR4[（182.20±61.59）vs.（125.10±61.9）,P〈0.01],TNF-α（52.62±19.04）vs.（32.63±13.71）ng/L,P〈0.01）。再狭窄组术后TLR4和TNF-α均升高,与支架置入术前相比差异有统计学意义;术后血清中TNF-α的浓度与外周血单核细胞中TLR4表达的平均荧光强度呈正相关。结论：冠状动脉支架置入术后外周血TLR4及TNF-α的表达均升高,且再狭窄组升高更明显,与无再狭窄组比较,差异有统计学意义。推测TLR4及TNF-α介导的炎症反应与支架术后再狭窄相关。 Objective：In-stent restenosis（ ISR） is one of the major limitations of percutaneous coronary intervention（ PCI）. Here,our aim is to investigate the relationship of peripheral blood toll like receptor 4（ TLR4） and TNF-α with in-stent restenosis after coronary stent implantation. Methods： The study population consisted of 135 patients assessed by coronary angiography with single-vessel disease and underwent stent implantation into narrowed coronary segments. Patients were divided into 2 groups according to the angiographic study after 6 to 12 months follow-up： those with coronary in-stent restenosis and those without coronary in-stent restenosis. In addition,the evaluation of TLR4 level by flow cytometry and TNF-α level by ELISA method before PCI and 5-7 days after PCI was performed. Results： 14 patients（ 10. 4%） developed in-stent restenosis after 6-12 months follow up and 121（ 89. 6%） without ISR. There was no difference of the level of TLR4 and TNF-α before PCI between patients with and without ISR [TLR4：（ 144. 20 ± 52. 99） vs.（ 117. 40 ± 61. 9）,P〈0.05]; TNF-α： [（ 34. 32 ± 11. 97） vs.（ 27. 47 ± 14. 47） ng /L,P〈0.05）. Patients with ISR were characterized by significantly higher surface expression of TLR4 and serum concentration of TNF-α after PCI [TLR4：（ 182.20 ±61.59）; TNF-α：（ 52.62 ±19.04） ng/L） than patients without ISR,TLR4：（ 125.10 ±61.9）;TNF-α：（ 32. 63 ± 13. 71） ng /L,P〈0.01]. TLR4 expression correlated positively with plasma TNF-α level in patients with ISR after PCI. Conclusion： We demonstrate that elevated TLR4 and TNF-α after PCI are associated with coronary in-stent restenosis.

作者马克娟郝蓬方冬平何东方赵林卢春山张英川郭成军

机构地区首都医科大学附属北京安贞医院北京市心肺血管疾病研究所心内

出处《心肺血管病杂志》 CAS 2014年第5期678-682,共5页 Journal of Cardiovascular and Pulmonary Diseases

基金国家自然科学基金青年项目(81200140)

关键词 TOLL样受体4 TNF-Α 冠心病经皮冠状动脉介入治疗支架置入术后再狭窄 Toll like receptor 4 TNF-α Coronary artery disease Percutaneous coronary intervention In-stent restenosis

分类号 R54 [医药卫生—心血管疾病]

引文网络
相关文献

参考文献16

1Jukema JW,Verschuren JJ,Ahmed TA,et al.Restenosis after PCI.Part 1:pathophysiology and risk factors.Nat Rev Cardiol,2011,9:53-62.
2Dibra A,J Mehilli SB,Hadamitzky H,et al.Inflammatory response after intervention assessed by serial C-reactive protein measurements correlates with restenosis in patients treated with coronary stenting.Am Heart J,2005,150:344-50.
3Blum A,Kaplan G,Vardinon N,et al.Serum amyloid type A may be a predictor of restenosis.Clin Cardiol,1998,21:655-658.
4Hojo Y,Ikeda U,Katsuki T,et al.Interleukin 6 expression in coronary circulation after coronary angioplasty as a risk factor for restenosis.Heart,2000,84:83-88.
5Akira S,Takeda K,Kaisho T.Toll-like receptors:critical proteins linking innate and acquired immunity.Nat Immunol,2004,4:499-511.
6Edfeldt K,Swedenborg J,Hansson GK,et al.Expression of tolllike receptors in human atherosclerotic lesions:a possible pathway for plaque activation.Circulation,2002,105:1158-1161.
7Kawai T,Akira S.The role of pattern-recognition receptors in innate immunity:update on Toll-like receptors.Nat Immunol,2010,11:373-384.
8Smiley ST,King JA,Hancock WW.Fibrinogen stimulates macrophage chemokine secretion through toll-like receptor 4.J Immunol,2001,167:2887-94.
9de Graaf R,Kloppenburg G,Kitslaar PJ,et al.Human heat shock protein 60 stimulates vascular smooth muscle cell proliferation through Toll-like receptors 2 and 4.Microbes Infect,2006,8:1859-65.
10Moghimpour Bijani F,Vallejo JG,Rezaei N.Toll-like receptor signaling pathways in cardiovascular diseases:challenges and opportunities.Int Rev Immunol,2012,31:379-95.

二级参考文献20

1杨永宗.中国动脉粥样硬化病理生理学研究近况[J].中国动脉硬化杂志,2004,12(4):481-489. 被引量：33
2赵一俏,傅强,李志梁,严全能,吴宏超,缪绯,吕永恒,刘映峰.冠心病患者外周血CD4^+CD28^-T细胞和CD4^+CD25^+T细胞亚群变化[J].南方医科大学学报,2007,27(4):474-476. 被引量：6
3Hye JH,Jong WH,Boyoung J,et al.Relation of inflammationand left atrial remodeling in atrial fibrillation occurring in earlyphase of acute myocardial infarction.Int J Cardiol,2011,146:28-31.
4Yoshinori N,Yoshihiro Y,Hideki S,et al.The effect of edara-vone on plasma monocyte chemoattractant protein-1 levels in pa-tients with acute myocardial infarction.J Cardiol,2009,54:416-424.
5Hirofumi S,Hisao O,Hirofumi Y,et al.Angiotensin-convertingenzyme inhibition reduces monocyte chemoattractant protein-1and tissue factor levels in patients with myocardial infarction.JAm Coll Cardiol,1999,34:983-988.
6Zhang ZX,Gao FY,Li KM,et al.Effect of magnesium litho-spermateB on endothelial cells in human aort a after fr ee r adical injury.Zhong Guo Zhong Xi Yi Jie He Za Zhi,2004,24:521-524.
7Antman EM,Anbe DT,Armstrong PW,et a.l ACC/AHAGuidelines for the management of patients with ST elevation myo-cardial infarction:A report of the am erican C ollege of cardiolo-gy/American heart association task force on practice(Committeeto revise the 1999 guidelines for the management of patients withacute myocardial infarct ion).J Am Coll Cardiol,2004,44:12-211.
8Manuel G,JoséA R,Matías PP,et al.Effect of the early ad-ministration of pravastatin on C-Reactive protein and interleukin-6 levels in the acute phase of myocardial infarction with ST seg-ment elevation.Rev Esp Cardiol,2004,57:916-923.
9Keiko T,Kentaro S,Masayuki Y.SDF-1-induced adhesion ofmonocytes to vascular endothelium is modulated by azelnidipinevia protein kinase C inhibition.Eur J Pharmacol,2006,522:162-169.
10Basri A,Sedat K,Hurkan K,et al.Monocyte chemoattractantprotein-1 in acute coronary syndromes:Complex vicious interac-tion.Int J Cardiol,2009,136:356-357.