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心力衰竭患者血浆中细胞凋亡抑制因子和细胞因子的变化以及阿托伐他汀的干预作用 被引量:12

Level of plasma soluble Fas and cytokines in patients with chronic heart failure and the effects of atorvastatin
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摘要 目的:观察阿托伐他汀对心力衰竭患者血浆中细胞凋亡抑制因子(sFas)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及超敏C反应蛋白(hs-CRP)水平的影响,探讨阿托伐他汀对心力衰竭的治疗作用。方法:将60例心力衰竭患者随机分为对照组和干预组,采用酶联免疫吸附法测定其治疗前后血浆中sFas、TNF-α、IL-6、hs-CRP水平。结果:左室射血分数(LVEF)≤30%者较>30%者sFas水平明显升高(P<0.05),sFas与LVEF及左室短轴缩短率(FS)呈显著负相关(r=-0.425,P<0.01),(r=-0.309,P<0.05)。hs-CRP水平在心功能Ⅳ级明显高于心功能Ⅲ级。TNF-α水平2组治疗后均较治疗前有显著下降(P<0.01或0.05),干预组较对照组下降更明显(P<0.05)。对照组血浆sFas水平较治疗前明显降低(P<0.05)而干预组治疗前后没有明显变化。干预组血浆IL-6水平较治疗前明显降低(P<0.05)。结论:在常规治疗的基础上加用阿托伐他汀可进一步降低心力衰竭患者血浆中TNF-α、IL-6等细胞因子水平,提示阿托伐他汀具有抗炎保护心肌作用;但阿托伐他汀可能影响Fas/FasL系统活性而促进心肌细胞凋亡,对患者产生不利影响。 Objective:To observe the influence of atorvastatin on cardiac function and plasma levels of sFas, tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) in patients with heart failure and investigate the therapeutic action of atorvastatin on heart failure. Methods: Sixty patients with heart failure were randomized to conventional or conventional plus atorvastatin groups. The plasma levels of sFas, TNF-αand IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) before management and were re-measured after two weeks' therapy. Result :The plasma sFas levels in the patients whose ejection fraction (EF) less than 30 % were significantly higher than in patients with EF more than 30% ( P 〈0.05). The sFas levels were correlated negatively to EF ( r = - 0. 425, P 〈0.01) and FS ( r = -0. 309, P 〈0.05). The serum hs-CRP levels in the New York Heart Association class Ⅳ patients were significantly higher than NYHA class Ⅲ patients. The plasma TNF-αlevels were significantly decreased in both groups after therapy ( P 〈0. 01 -0.05). The decreaing extent of TNF-α in the atorvastatin-treated group was greater than in the conventional group ( P 〈0.05). The plasma levels of sFas were significantly descented after therapy in the conventional group ( P 〈0.05) and there was no obvious change in the atorvastatin-treated group. The plasma levels of IL-6 were significantly descented after therapy in the atorvastatintreated group ( P 〈0.05). Conclusion:The treatment of conventional plus atorvastatin might generate anti-inflammatory effects and protect myocardium by decrease the plasma levels of pro-inflammatory cytokines such as TNF-α and IL-6. But atorvastatin could promote myocardial apoptosis through influence the activity of Fas/sFasL system and result in adverse effects on patients. The advantageous effects of atorvastatin on heart failure treatment may be greater than detrimental effects.
出处 《临床心血管病杂志》 CAS CSCD 北大核心 2007年第2期97-100,共4页 Journal of Clinical Cardiology
关键词 心力衰竭 阿托伐他汀 细胞凋亡抑制因子 肿瘤坏死因子-α 白细胞介素-6 Heart failure Atorvastatin sFas Tumor necrosis factor-α Interleukin-6
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参考文献18

  • 1FRANCIS G S. Neurohumoral activation and progression of heart failure., hypothetical and clinical consideration[J]. J Cardiovasc Pharmacol, 1998, 32: 16-21.
  • 2SHAROV V G, SABBAH H N, SHIMOYAMA H,et al. Evidence of cardiocyte apoptosis in myocardium of dogs with chyonic heart failure[J]. Am J Pathol,1996, 148: 141-149.
  • 3SARASTE A, VIOPIOPULKKI L M, PARVINEN M, et al. Apoptosis in the heart[J]. N Engl,J Med,1997, 336: 1025-1026.
  • 4SCHUMANN H, MORAWIETZ H, KAVOUS H,et al. Alternative splicing of the primary Fas transcript generating soluble Fas antagonists is suppressed in the failing human ventricular myocardium[J]. Biochem Biophys Res Commun, 1997, 239 : 794-798.
  • 5LIU Y, CIGOTA E, CHENG W, et al. Myocyte unclear mitotic divisio and programmed myocyte cell death characterize the cardiac myopathy induced by rapid ventrieular pacing in dogs [J]. Lab Invest,1995, 73: 771-778.
  • 6CHENG W, BAOSHENG L, KAJSTURA J, et al.Stretch-induced programmed myocyte cell death[J]. J Clin Invest, 1995, 96:2247-2259.
  • 7NISHIGAKI K, MINATOGUCHI S, SEISHIMA M, et al. Plasma Fas ligand, an inducer of apoptosis,and plasma soluble Fas, an inhibitor of apoptosis, inpatients with chronic congestive heart failure[J]. J Am Coil Cardiol, 1997, 29:1214-1220.
  • 8OKUYAMA M, YAMAGUCHI S, NOZAKI N, et al. Serum levels of soluble form of Fas molecule in patients with congestive heart failure[J]. Am J Cardiol,1997, 79: 1698-1701.
  • 9KAWAKAMI H, SHIGEMATSU Y, OHTSUKA T, et al. Increased circulating soluble form of Fas in patients with dilated cardiomyopathy[J]. Jpn Circ J,1998, 62: 873-876.
  • 10YAMAGUCHI S, YAMAOKA M, OKUYAMA M,et al. Elevated circulating levels and cardial secretion of soluble Fas ligand in patients with congestive heart failure[J]. Am J Cardiol, 1999, 83: 1500-1503.

二级参考文献19

  • 1Karas RH. Statin use enhances coronary collaterals[J]. Am Heart J, 2003,146: 876-881.
  • 2Pliquett RU, Cornish KG, Peuler JD, et al. Simvastatin normalizes autonomic neural control in experimental heart failure [J]. Circulation, 2003,107: 2493-2498.
  • 3Grip O, Janciauskiene S, Lindgren S. Pravastatin down-regulates inflammatory mediators in human monocytes in vitro [J]. Eur J Pharmacol, 2000,410: 83-92.
  • 4Maack C, Kartes T, Kilter H, et al. Oxygen free radical release in human failing myocardium is associated with increased activity of racl-GTPase and represents a target for statin treatment[J]. Circulation, 2003,108: 1567-1574.
  • 5Segal R,Fiebeler A,Park JK, et al. Amelioration of angiotensin Ⅱ-induced cardiac injury by a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor[J]. Circulation, 2001,104:576-581.
  • 6Node K. Short-term statin therapy improves cardiac function and symptoms in patients with idiopathic dilated cardiomyopathy[J]. Circulation, 2003,108: 839-843.
  • 7Katta M, Alexander BS, Krichten CM, et al. The effect of coenzyme Q10 in patients with congestive heart failure [J]. Ann Intern Med, 2000,132:636-640.
  • 8Rauchhaus M, Clark AL, Doehner W, et al. The relationship between cholesterol and survival in patients with chronic heart failure [J]. J Am Coll Cardiol,2003,42:1933-1940.
  • 9Fonarow G, Horwich TB. Cholesterol and mortality in heart failure: the bad gone good[J]? J Am Coll Cardiol,2003,42: 1941-1943.
  • 10Colucci,WS.Molecular and cellular mechanisms of myocardial failure[].The American Journal of Cardiology.1997

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