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男性心力衰竭患者血清雄激素与细胞因子及活化蛋白的关系 被引量:3

Association of serum androgen level with cytokines and activator protein-1 in male chronic heart failure patients
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摘要 目的探讨男性心力衰竭(心衰)患者血清雄激素与细胞因子及活化蛋白(activator protein-1,AP-1)的关系。方法选择160例男性心衰患者作为心衰组,心功能(NYHA)Ⅱ级40例,Ⅲ级55例,Ⅳ级65例,同期选择40例健康体检男性作为对照组,ELISA法检测外周血游离睾酮(FT)、总睾酮(TT)、去氢表雄酮(DHEA)、去氢表雄酮硫酸酯(DHEAS),白细胞介素(IL)-1β、IL-6、TNF-α、IL-10及AP-1的水平,进行相关分析。结果心衰组血清FT[(42.76±8.46)pmol/L vs(51.25±4.71)pmol/L]、TT[(14.26±3.65)nmol/L vs(17.98±2.59)nmol/L]、DHEA[(6.63±1.43)nmol/Lvs(6.39±1.39)nmol/L]、DHEAS[(1.77±0.59)nmol/Lvs(2.28±0.43)nmol/L]及IL-10水平显著低于对照组,随心功能Ⅱ级、Ⅲ级到Ⅳ级增加逐级显著下降(P<0.05,P<0.01)。心衰组血清IL-1β、IL-6、TNF-α、AP-1水平显著高于对照组,由心功能Ⅱ级、Ⅲ级到Ⅳ级增加而逐级显著升高(P<0.05,P<0.01)。心衰组FT、TT、DHEA、DHEAS与IL-1β、IL-6、TNF-α、AP-1呈负相关(P<0.05,P<0.01),与IL-10呈正相关(P<0.05,P<0.01);FT与AP-1独立负相关(P<0.01)。结论男性心衰患者血清雄激素水平减低,可能与致炎细胞因子增高、抗炎细胞因子减少及AP-1活化有关,低雄激素血症影响男性心衰的发生和发展。 Objective To study the association of serum androgen level with cytokines and activator protein-1 (AP-1) in male chronic heart failure (CHF) patients. Methods One hundred and sixty male CHF patients served as a CHF group and 40 healthy male subjects served as a control group in this study. Their serum levels of free testosterone (FT),total testosterone (TT),dehydroepi androsterone (DHEA),dehydro-epiandrosterone sulfate (DHEAS),IL-1β,II76 ,TNF-α,IL-10 and AP 1 were measured by ELISA and their association was analyzed. Results The serum levels of FT,TT,DHEA,DHEAS,IL-10 were significantly lower in CHF group than in control group and decreased with the increased NYHA classification from Ⅱ to Ⅲ and Ⅳ (P〈0.05,P〈0.01). The serum levels of IL-1β,IL-6,TNF-α,AP 1 were significantly higher in CHF group than in control group and increased with the increased NYHA classification from Ⅱ to Ⅲ and Ⅳ (P〈0.05,P〈0.01). The serum levels of FT,TT,DHEA,DHEAS were negatively related with those of IL-1β, IL- 6,TNF-α,AP-1 (P〈0.05,P〈0.01) and positively related with that of IL-10 (P〈0.05,P〈0.01). The serum FT level was independently and negatively associated with that of AP-1 (P〈 0.01). Conclusion Low serum androgen level in male CHF patients is associated with increased proinflammatory cytokines, decreased antiinflammatory cytokines and activated AP-1. Hypoandrogenism have an adverse offect on the occurrence and development of CHF in males.
出处 《中华老年心脑血管病杂志》 CAS 2015年第2期146-149,共4页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词 心力衰竭 雄激素类 细胞因子类 睾酮 白细胞介素10 白细胞介素6 heart failure androgens cytokines testosterone interleukin-10 interleukin-6
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参考文献13

  • 1Hill C, Wurfel A, Heger J, et al. Inhibition of AP 1 signaling by JDP2 overexpression protects cardiomyocytes against hy pertrophy and apoptosis induction. Cardiovasc Res, 2013,99 : 121- 128.
  • 2陈倩,李小鹰,李江源,张万义,李洪涛,刘芳.老年男性心力衰竭患者性激素水平调查及与同龄健康男性的比较[J].中华心血管病杂志,2005,33(6):505-508. 被引量:34
  • 3Guder G, Frantz S, Bauersachs J, et al. Low circulating andro- gens and mortality risk in heart failure. Heart, 2010,96:504 -509.
  • 4Musa M, Fernando SM, Chatterjee D, et al. Subcellular effects of myocyte specific androgen receptor overexpression in mice. J Endocrinol,2011,210:93- 104.
  • 5Wrigley BJ, Lip GY, Shantsila E. The role of monocytes and inflammation in the pathophysiology of heart failure. Eur J Heart Fai1,2011,13:1161- 1171.
  • 6Niu J, Azfer A, Deucher MF, et al. Targeted cardiac expres sion of soluble Fas prevents the development of heart failure in mice with cardiac specific expression of MCP-1. J Mol Cell Cardiol, 2006,40 : 810-820.
  • 7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
  • 8Pfeilschifter J, Koditz R, Pfohl M, et al. Changes in proinflam matory eytokine activity after menopause. Endocr Rev, 2002, 23:90 -119.
  • 9Malkin CJ, Pugh PJ, Jones RD, et al. Testosterone as a pro tective factor against atherosclerosis immunomodulation and influence upon plaque development and stability. J Endocri nol, 2003,178 : 373-380.
  • 10Yesilova Z, Ozata M, Kocar IH, et al. The effects of gonado tropin treatment on the immunological features of male pa tients with idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab,2000,85:66- 70.

二级参考文献28

  • 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.

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