C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular diseases

Li, Jianjun; Fang, Chuo

doi:10.1016/j.mehy.2003.12.014

Cited by 188 publications

(110 citation statements)

References 51 publications

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“…These inflammatory factors stimulate the liver and CRP is secreted by the liver in response to a variety of inflammatory cytokines. CRP further stimulates the release of Il-6 and TNF-a, accelerating injury to the blood vessels [17]. In our study, occlusion of the coronary artery was associated with increased serum levels of TNF-a and Il-6 ( Fig.…”

Section: Discussionsupporting

confidence: 53%

Anti-Inflammatory Effect of Guan-Xin-Er-Hao via the Nuclear Factor-Kappa B Signaling Pathway in Rats with Acute Myocardial Infarction

et al. 2010

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Abstract:A traditional Chinese medicine, Guan-Xin-Er-Hao (GXEH), is a famous multiple target therapeutic polypharmaceutical. Our aim was to evaluate whether or not oral administration of GXEH has an anti-inflammatory effect associated with blockade of nuclear factor-kappa B (NF-κB), and to investigate the NF-κB-mediated pro-inflammatory cytokines expression pathway during acute myocardial infarction (AMI) in rats. Sprague-Dawley rats were randomly assigned to four groups: oral GXEH administered at 15 or 5 g/kg, the vehicle control and sham-operated groups. Thirty minutes after giving GXEH or 0.9% NaCl (p.o.) once, coronary arteries were occluded except for the sham-operated rats. We measured 24-h infarct size, 3-h expression of NF-κB protein in the myocardial left ventricular tissues and serum levels of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and C-reactive protein (CRP). Compared with rats receiving vehicle, rats administered 15 g/kg GXEH had significantly reduced 24-h infarct size, expression of NF-κB protein and serum concentrations of TNF-a, IL-6, and CRP. GXEH at 5 g/kg did not have a significant effect on these parameters. In conclusion, GXEH exhibited an anti-inflammatory effect through inhibition of the NF-κB-mediated signaling pathway leading to downregulation of pro-inflammatory cytokine expression. These findings provide new evidence of the cardioprotective effect of GXEH through reduction of infarct size by mediating lots of endogenous materials via multiple pathways to act on myocardial cells in the treatment of cardiovascular disease.

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Section: Discussionsupporting

confidence: 53%

Anti-Inflammatory Effect of Guan-Xin-Er-Hao via the Nuclear Factor-Kappa B Signaling Pathway in Rats with Acute Myocardial Infarction

et al. 2010

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“…However, at higher concentrations, aspirin has also been shown to block NF-kB activity by directly binding to and inhibiting the kinase activity of IKKb by reducing its ability to bind ATP (Yin et al, 1998); more recently, aspirin has also been reported to inhibit proteasome activity and consequently to interfere with degradation of IkB (Dikshit et al, 2006). As such, high-dose aspirin therapy may have applications to diseases where NF-kB activity is involved, including cancer (McCarty and Block, 2006), diabetes (Yuan et al, 2001) and heart disease (Li and Fang, 2004).…”

Section: Anti-inflammatory Drugsmentioning

confidence: 99%

Inhibitors of NF-κB signaling: 785 and counting

2006

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“…In addition, a large amount of data indicated that C-reactive protein (CRP), a sensitive marker of underlying systemic inflammation, is increased among men and women at risk for future cardiovascular events, and the addition of CRP testing to standard lipid screening seems to provide an improved method to determine vascular risk (12). Vila et al (13) demonstrated that plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) is increased in a model of systemic infection/inflammation in healthy men with normal heart function.…”

Section: Introductionmentioning

confidence: 99%

Acute phase reactants in patients with coronary slow flow phenomenon

Madak¹,

Nazlı²,

Mergen³

et al. 2010

Anadolu Kardiyol Derg

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Acute phase reactants in patients with coronary slow flow phenomenonKoroner yavaş akım fenomeni olan hastalarda akut faz reaktanları 416ABSTRACT Objective: In this study, we sought to investigate the serum levels of high sensitivity C-reactive protein (Hs-CRP), N-terminal pro-brain natriuretic peptide (NT proBNP), erythrocyte sedimentation rate, leukocyte, thyroid hormone and fibrinogen levels in patients with coronary slow flow phenomenon (CSFP). Methods: A total of 82 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (45 males and 37 females, mean age 59±11 years) and 34 patients with normal coronary arteries and normal coronary flow (19 males and 15 females, mean age 56±10 years) with similar risk profiles were included in this cross-sectional observational study. Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction (TIMI) frame count, serum level of Hs-CRP, NT proBNP, sedimentation, leukocyte, free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH) and fibrinogen levels were measured. Statistical analysis was performed using t test for independent samples, Chi-square test and Pearson correlation analysis.Results: Hs-CRP (0.88±0.86 vs 0.36±0.35 mg/L, p<0.001) and NT proBNP (117.83±163.2 vs 47.33±30.6 ng/ml, p<0.01) were found to be significantly higher in patients with coronary slow flow compared with normal control group. There were no significant differences regarding thyroid hormones, fibrinogen, sedimentation rate and leukocyte count between two groups. The mean TIMI frame counts were positively correlated (r=0.454, p=0.001 and r=0.554, p=0.001, respectively) with plasma Hs-CRP levels and NT-proBNP levels.

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C-reactive protein is not only an inflammatory marker but also a direct cause of cardiovascular diseases

Cited by 188 publications

References 51 publications

Anti-Inflammatory Effect of Guan-Xin-Er-Hao via the Nuclear Factor-Kappa B Signaling Pathway in Rats with Acute Myocardial Infarction

Anti-Inflammatory Effect of Guan-Xin-Er-Hao via the Nuclear Factor-Kappa B Signaling Pathway in Rats with Acute Myocardial Infarction

Inhibitors of NF-κB signaling: 785 and counting

Acute phase reactants in patients with coronary slow flow phenomenon

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