Circulating Interleukin-1 Beta, Interleukin-6, Tumor Necrosis Factor-Alpha, and Soluble ICAM-1 in Patients with Chronic Stable Angina and Myocardial Infarction

Balbay, Yücel; Tıkız, Hakan; Baptiste, R.J.; Ayaz, Selime; Şaşmaz, Hatice; Korkmaz, Şule

doi:10.1177/000331970105200204

Cited by 57 publications

(34 citation statements)

References 24 publications

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“…The mRNA and protein expressions of IL-1β and TNF-α in the brains were markedly lower, but the mRNA and protein expressions of IL-10 and IL-10R in the brains were markedly higher in the GbE 100 mg/kg group than that in the AS group. Our results were consistent with the recent findings that the serum levels of TNF-α and IL-1β in all patients with coronary heart diseases were higher than those in controls [7][8][9] . IL-10 was an anti-inflammatory cytokine with powerful immunoregulation potential [10] .…”

Section: Discussionsupporting

confidence: 93%

Expression of pro-inflammatory and anti-inflammatory cytokines in brain of atherosclerotic rats and effects of Ginkgo biloba extract1

Jiao

Rui

et al. 2005

Acta Pharmacologica Sinica

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Aim: To study the protein and mRNA expressions of pro-inflammatory and antiinflammatory cytokines in the brain of rats with atherosclerosis (AS) and the effects of Ginkgo biloba extract (GbE) on expressions of cytokines. Methods: The experimental model of AS in rats were established by intraperitioneal injection of vitamin D 3 with high fat/cholesterol diet. GbE 100 mg/kg was administered to rats by ig. After 8 weeks, the expressions of IL-1β, TNF-α, IL-10, and IL-10R in the brain tissues of AS rats were detected by enzyme-linked immunosorbant assay, immunohistochemistry, Western blotting, and reverse transcriptase polymerase chain reaction. Results: The protein and mRNA expressions of IL-1β, TNF-α, and IL-10 in the brains were markedly higher in AS groups than that in control groups (6.11±0.15, 1.55±0.14, 0.54±0.04 ng/g wet weight vs 0.80±0.14, 0.33±0.09, and 0.33±0.02 ng/g wet weight, respectively). The protein and mRNA expressions of IL-1β and TNF-α in the brains were markedly lower in GbE groups (3.82±0.54, 0.95±0.08 ng/g wet weight) than that in AS groups, the protein and mRNA expressions of IL-10 and IL-10R in the brains were markedly higher in GbE groups (0.85±0.06 ng/g wet weight) than that in AS groups. Conclusion: GbE inhibited production of pro-inflammatory cytokines IL-1β and TNF-α, but upregulated the production of anti-inflammatory cytokines, IL-10 and IL-10R in brain, which might be related with its anti-AS actions.

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Section: Discussionsupporting

confidence: 93%

Expression of pro-inflammatory and anti-inflammatory cytokines in brain of atherosclerotic rats and effects of Ginkgo biloba extract1

Jiao

Rui

et al. 2005

Acta Pharmacologica Sinica

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“…The present study has demonstrated elevation of plasma levels of TNF-a and IL-6 as a result of AMI, which is in accord with many prior reports [3][4][5]15,17,[19][20][21][22][23][24][25][26]. The time course of cytokine activation in AMI reflected by increased gene expression in heart muscle or elevated plasma concentrations varied from 2 to 40 days in different studies [2,[26][27][28][29][30][31].…”

Section: Discussionsupporting

confidence: 92%

“…IL-6 depresses myocardial function predominantly by activation of iNOS and partially by stimulation of intercellular cell adhesion molecule (ICAM-1) with accumulation of neutrophiles and subsequent neutrophile-dependent myocardial injury [1,[14][15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory cytokines and myocardial viability in patients after acute myocardial infarction

Kosmala

Przewlocka‐Kosmala

Mazurek

2005

International Journal of Cardiology

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“…Other data from the same study groups (62) and data from an additional study of early effects of ICV SL (60) suggest that the SL acts centrally to reduce sympathetic drive in HF rats. failure and MI literature, the most studied of the proinflammatory cytokines are TNF-␣, interleukin-6, and interleukin-1␤ (6,38,39,84,118,131). In our rat model (61), blood-borne TNF-␣ increases as early as 30 min after coronary artery ligation.…”

Section: The Cytokine Connectionmentioning

confidence: 99%

Heart failure and the brain: new perspectives

Felder¹,

Francis²,

Zhang³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

109

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Heart failure and the brain: new perspectives. Am J Physiol Regul Integr Comp Physiol 284: R259-R276, 2003; 10.1152/ajpregu.00317.2002.-Despite recent therapeutic advances, the prognosis for patients with heart failure remains dismal. Unchecked neurohumoral excitation is a critical element in the progressive clinical deterioration associated with the heart failure syndrome, and its peripheral manifestations have become the principal targets for intervention. The link between peripheral systems activated in heart failure and the central nervous system as a source of neurohumoral drive has therefore come under close scrutiny. In this context, the forebrain and particularly the paraventricular nucleus of the hypothalamus have emerged as sites that sense humoral signals generated peripherally in response to the stresses of heart failure and contribute to the altered volume regulation and augmented sympathetic drive that characterize the heart failure syndrome. This brief review summarizes recent studies from our laboratory supporting the concept that the forebrain plays a critical role in the pathogenesis of ischemiainduced heart failure and suggesting that the forebrain contribution must be considered in designing therapeutic strategies. Forebrain signaling by neuroactive products of the renin-angiotensin system and the immune system are emphasized.angiotensin; aldosterone; cytokines; tumor necrosis factor; immune system; renin; vasopressin; sympathetic; extracellular fluid volume; baroreflex THE IMPORTANCE OF AUTONOMIC dysfunction to the progression of heart failure is firmly established (55,113,120,152). The most effective treatments for heart failure specifically target the peripheral manifestations of neurohumoral activation (86,113). Yet the understanding of the mechanisms leading to neurohumoral excitation in heart failure is still quite limited.Over the last several decades, substantial evidence has been amassed to support the concept that peripheral afferent systems innervating the heart and vascular tree are altered in heart failure. Dysfunction has been described in all components of the reflexes mediated by these cardiovascular afferent systems-the afferent fibers themselves, the central processing of the afferent signals, the efferent innervation of the end organs, and the end organs themselves. In general, the influence of low-and high-pressure baroreceptors (40,42,191) that normally restrain sympathetic drive and vasopressin release is diminished, whereas the excitatory influences of arterial chemoreceptors (161) and cardiac sympathetic afferent fibers (100) are enhanced.Central nervous system (CNS) neurons affecting cardiovascular regulation respond to humoral as well neural signals. Blood-borne neuroactive peptides, too large to readily cross the blood-brain barrier, may influence the brain by activating sensory neurons at specific sites in hindbrain and forebrain that lack a blood-brain barrier (15,18) or by inducing the release of mediators that do penetrate the barrier (135). These neuroactive s...

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Circulating Interleukin-1 Beta, Interleukin-6, Tumor Necrosis Factor-Alpha, and Soluble ICAM-1 in Patients with Chronic Stable Angina and Myocardial Infarction

Cited by 57 publications

References 24 publications

Expression of pro-inflammatory and anti-inflammatory cytokines in brain of atherosclerotic rats and effects of Ginkgo biloba extract1

Expression of pro-inflammatory and anti-inflammatory cytokines in brain of atherosclerotic rats and effects of Ginkgo biloba extract1

Proinflammatory cytokines and myocardial viability in patients after acute myocardial infarction

Heart failure and the brain: new perspectives

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