scholarly journals Cardiorenal Syndrome in Hypertensive Rats: Microalbuminuria, Inflammation and Ventricular Hypertrophy

2012 ◽  
pp. 13-24 ◽  
Author(s):  
M. MOUBARAK ◽  
H. JABBOUR ◽  
V. SMAYRA ◽  
E. CHOUERY ◽  
Y. SALIBA ◽  
...  
Keyword(s):  
Ventricular Hypertrophy ◽  
Cardiorenal Syndrome ◽  
Left Ventricular ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Factor Alpha ◽  
Low Grade Inflammation

The aim of our study was to evaluate a possible association between microalbuminuria (MA), several low-grade inflammation factors and left ventricular hypertrophy (LVH) by using a pharmacological approach. This may provide new insights into the pathophysiologic mechanisms of the cardiorenal syndrome (CRS) linking early renal impairment with elevated cardiovascular risk. Two kidney-one clip (2K-1C) renovascular hypertension was induced in 24 male Wistar rats (220-250 g). After the development of hypertension, rats were divided into four groups: 2K-1C (untreated), calcium channel blocker (amlodipine-treated), angiotensin receptor blocker (losartan-treated) and peripheral vasodilator (hydralazine-treated), which were treated for 10 weeks. Rats in the 2K-1C group had all developed hypertension, a significant increase in plasma levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), brain natriuretic peptide (BNP) and C-reactive protein (CRP). Moreover MA and creatininaemia underwent a significant increase. Under treatment decreases were observed in systolic blood pressure (SBP), TNF-α, CRP, IL-6, BNP concentrations and creatininaemia. These results were related to the absence of MA which was significantly associated with reductions in cardiac mass and hypertrophy markers (BNP and β-MHC gene expression) as well as renal interstitial inflammation. In conclusion, our results suggest that the reduction of MA is correlated with the decrease of the inflammatory components and seems to play an important role in protecting against cardiac hypertrophy and renal injury.

scholarly journals Low-grade inflammation and tryptophan-kynurenine pathway activation are associated with adverse cardiac remodeling in primary hyperparathyroidism: the EPATH trial

2017 ◽  
Vol 55 (7) ◽  
Author(s):  
Nicolas Verheyen ◽  
Andreas Meinitzer ◽  
Martin Robert Grübler ◽  
Klemens Ablasser ◽  
Ewald Kolesnik ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Primary Hyperparathyroidism ◽  
Cardiac Remodeling ◽  
Ventricular Hypertrophy ◽  
Kynurenine Pathway ◽  
Left Ventricular ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Low Grade Inflammation

AbstractBackground:Primary hyperparathyroidism (pHPT) is associated with low-grade inflammation, left ventricular hypertrophy and increased cardiovascular mortality, but the association between inflammatory markers and parameters of adverse cardiac remodeling is unknown. We investigated the relationship between C-reactive protein (CRP), the essential amino acid tryptophan and its pro-inflammatory derivatives kynurenine and quinolinic acid (QUIN) with echocardiographic parameters.Methods:Cross-sectional baseline data from the “Eplerenone in Primary Hyperparathyroidism” trial were analyzed. Patients with any acute illness were excluded. We assessed associations between CRP, serum levels of tryptophan, kynurenine and QUIN and left ventricular mass index (LVMI), left atrial volume index (LAVI) and E/e′.Results:Among 136 subjects with pHPT (79% females), 100 (73%) had arterial hypertension and the prevalence of left ventricular hypertrophy was 52%. Multivariate linear regression analyses with LVMI, LAVI and E/e′ as respective dependent variables, and C-reactive protein and tryptophan, kynurenine and QUIN as respective independent variables were performed. Analyses were adjusted for age, sex, blood pressure, parathyroid hormone, calcium and other cardiovascular risk factors. LVMI was independently associated with CRP (adjusted β-coefficient=0.193, p=0.030) and QUIN (β=0.270, p=0.007), but not kynurenine. LAVI was related with CRP (β=0.315, p<0.001), kynurenine (β=0.256, p=0.005) and QUIN (β=0.213, p=0.044). E/e′ was related with kynurenine (β=0.221, p=0.022) and QUIN (β=0.292, p=0.006). Tryptophan was not associated with any of the remodeling parameters.[Correction added after online publication (22 April 2017: The sentence “Among 136 subjects with pHPT (79% females), 100 (73%) had left ventricular hypertrophy.” was corrected to “Among 136 subjects with pHPT (79% females), 100 (73%) had arterial hypertension and the prevalence of left ventricular hypertrophy was 52%.”]Conclusions:Cardiac remodeling is common in pHPT and is associated with low-grade inflammation and activation of the tryptophan-kynurenine pathway. The potential role of kynurenine and QUIN as cardiovascular risk factors may be further investigated in future studies.

THE EFFECT OF ATORVASTATINUM IN THE TREATMENT OF PATIENTS WITH RHEUMATOID ARTHRITIS

2020 ◽  
Vol 73 (11) ◽  
pp. 2427-2430
Author(s):  
Sergii V. Shevchuk ◽  
Yuliia S. Seheda ◽  
Inna P. Kuvikova ◽  
Olena V. Shevchuk ◽  
Olena Y. Galiutina
Keyword(s):  
Inflammatory Process ◽  
Necrosis Factor Alpha ◽  
Traditional Treatment ◽  
Reactive Protein ◽  
Tnf Α ◽  
Endothelium Function ◽  
Factor Alpha ◽  
Inflammatory Drugs ◽  
Serum Paraoxonase ◽  
Necrosis Factor

The aim: Was to evaluate the effect of 6-month pathogenetic treatment in combination with atorvastatinum on the endothelium function, lipid and adipokine levels, paroxonase activity and activity of inflammatory process in RA patients. Materials and methods: The study included 55 patients with RA, dividing into two groups depending on the intended therapy. The first group included 33 patients with “traditional” treatment by methotrexate, glucocorticoids, and non-steroid anti-inflammatory drugs. The second group included 22 patients with “traditional” treatment and additionally prescribed of atorvastatinum 20 mg/day. The lipid profile, leptin, adipokine, paroxonase activity. C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) levels, FMDBA and IMT of carotid artery were determined in all participants of the study. Control parameters were recorded before the start, after 1 and 6 months of treatment. Results: The FMDBA has increased by 32% in the second group, compared by only 10.9% in the first group. The dynamics of IMT in the first group was also twice lower than in group with the additional use of atorvastatinum. The leptin levels in the second group significantly decreased by 27% and adiponectin levels increased by 12.8%, than in the first group – by 12.8% and by 7% respectively. The appointment of statins over 6 months resulted in DAS28, TNF-α, ESR and CRP reduction by 15%, 31%, 25% and 21.5% respectively. In the first group the dynamics of indicate rates ranged from 7.8% to 22.5%, and was significantly lower than in the second group. Conclusions: As a result of the study, it was found that the appointment of atorvastatinum 20 mg/day during 6 months not only reduces dyslipidemia, but also significantly reduces the inflammatory process and adipokine dysregulation, normalizes serum paraoxonase activity and improves the endothelium function.

scholarly journals Glucocorticoid Receptor Gene, Low-Grade Inflammation, and Heart Failure: The Heart and Soul Study

2010 ◽  
Vol 95 (6) ◽  
pp. 2885-2891 ◽  
Author(s):  
Christian Otte ◽  
Stefan Wüst ◽  
Shoujun Zhao ◽  
Ludmila Pawlikowska ◽  
Pui-Yan Kwok ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucocorticoid Receptor ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Low Grade ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Glucocorticoid Receptor Gene ◽  
Low Grade Inflammation

Abstract Context: A common haplotype of the glucocorticoid receptor (GR) gene has been associated with increased susceptibility to coronary heart disease (CHD). Whether this haplotype predisposes to heart failure (HF) is unknown. Objective: The objective of the study was to determine whether GR haplotype 3 is associated with HF and whether this association is explained by low-grade inflammation (C-reactive protein). Design: In a prospective cohort study, participants were genotyped for common GR gene polymorphisms (ER22/23EK, BclI C/G, N363S, 9β A/G). Haplotype analyses were conducted. Setting: The study was conducted at one university medical center, two Veterans Affairs medical centers, and nine public health clinics. Patients: Patients included 526 white outpatients with stable CHD. Main Outcome Measures: Echocardiographic evidence of ventricular dysfunction, self-reported heart failure, and subsequent hospitalization for heart failure were measured. Results: After adjusting for age, sex, smoking, and body mass index, participants with two copies of haplotype 3 were more likely than those with 0 or 1 copy to report heart failure [hazard ratio (HR) 4.15, 95% confidence interval (CI) 1.5–11.3, P &lt; 0.01], have systolic dysfunction (left ventricular ejection fraction &lt;50%) (HR 3.0, 95% CI 0.9–9.9, P = 0.07), and be hospitalized for HF during a mean follow-up of 6 yr (HR 3.0, 95% CI 1.3–7.0, P = 0.01). These associations were attenuated after adjustment for higher C-reactive protein levels in patients with two copies of haplotype 3. Conclusions: We found that the GR gene haplotype 3 was associated with prevalent HF, systolic dysfunction, and subsequent HF hospitalization in patients with CHD. This association was partly mediated by low-grade inflammation.

Low Grade Inflammation and ECG Left Ventricular Hypertrophy in Urban African Males: The SABPA Study

2013 ◽  
Vol 22 (11) ◽  
pp. 924-929 ◽  
Author(s):  
Carel van der Walt ◽  
Leoné Malan ◽  
Aletta S. Uys ◽  
Nicolaas T. Malan
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Low Grade ◽  
Low Grade Inflammation

scholarly journals HUBUNGAN HIPERURISEMIA DENGAN KARDIOMEGALI PADA PASIEN GAGAL JANTUNG KONGESTIF

e-CliniC ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Keishi G. D. Masengi ◽  
Jeffrey Ongkowijaya ◽  
Frans Wantania
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Necrosis Factor Alpha ◽  
Brain Center ◽  
Factor Alpha ◽  
Cardio Vascular ◽  
Necrosis Factor

Abstract: Hyperuricemia leads to left ventricular hypertrophy that affects the occurrence of congestive heart failure. Increased uric acid level causes increased production of reactive oxygen species (ROS). This ROS stimulates tumor necrosis factor-alpha (TNF-α) which binds to tumor necrosis factor receptor (TNFR) in the heart, causing a series of reactions of myocyte apoptosis and fibrosis with left ventricular hypertrophy as the final result. This study aimed to determine the relationship between hyperuricemia and cardiomegaly in patients with congestive heart failure. This was an analytical study with a cross sectional design. Samples were 30 patients with congestive heart failure hospitalized in Irina F and Cardio Vascular Brain Center Prof. Dr. R. D. Kandou Hospital in Manado. The result of independent T test stated that there was a significant association between hyperuricemia and cardiomegaly in patients with congestive heart failure with a p value 0,020 and an odds ratio of 3.571.Keywords: hyperuricemia, cardiomegaly, left ventricular hypertrophy, congestive heart failure Abstrak: Hiperurisemia menyebabkan terjadinya hipertrofi ventrikel kiri sehingga berdampak terjadinya gagal jantung kongestif. Peningkatan kadar asam urat menyebabkan peningkatan produksi reactive oxygen species (ROS). ROS akan menstimulasi tumour necrosis factor-alpha (TNF-α) yangs selanjutnya akan berikatan dengan tumour necrosis factor receptor (TNFR) di jantung sehingga menyebabkan serangkaian reaksi apoptosis miosit dan fibrosis dengan hasil akhir hipertrofi ventrikel kiri. Penelitian ini bertujuan untuk mengetahui hubungan hiperurisemia dengan kardiomegali pada pasien gagal jantung kongestif. Penelitian ini menggunakan metode analitik dengan desain potong lintang. Sampel penelitian ini ialah 30 pasien gagal jantung kongestif di rawat inap Irina F dan Cardio Vascular Brain Center RSUP Prof. Dr. R. D. Kandou Manado. Hasil Uji T Independent menyatakan bahwa ada hubungan bermakna antara hiperurisemia dan kardiomegali pada pasien gagal jantung kongestif (p=0,020), dengan nilai odds ratio sebesar 3,571.Kata kunci: hiperurisemia, kardiomegali, hipertrofi ventrikel kiri, gagal jantung kongestif

scholarly journals Delanzomib, a Novel Proteasome Inhibitor, Combined With Adalimumab Drastically Ameliorates Collagen-Induced Arthritis in Rats by Improving and Prolonging the Anti-TNF-α Effect of Adalimumab

2021 ◽  
Vol 12 ◽  
Author(s):  
Lei Wang ◽  
Lixiong Liu ◽  
Xiaoping Hong ◽  
Dongzhou Liu ◽  
Zeneng Cheng
Keyword(s):  
Proteasome Inhibitor ◽  
Proteasome Inhibitors ◽  
Collagen Induced Arthritis ◽  
Initial Finding ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level

Delanzomib is a novel proteasome inhibitor initially developed for treating multiple myeloma. It was found to inhibit the expression of tumor necrosis factor alpha (TNF-α). This study aimed to investigate the ameliorating effect of delanzomib on collagen-induced arthritis (CIA) and to explore the pharmacodynamics and pharmacokinetics (PK) interactions between delanzomib and adalimumab. Rats with CIA were randomly assigned to receive the treatment with delanzomib, adalimumab, delanzomib combined with adalimumab, or placebo. Visual inspection and biochemical examinations including TNF-α, interleukin 6, and C-reactive protein were performed to assess arthritis severity during the treatment. The adalimumab concentration in rats was determined to evaluate the PK interaction between delanzomib and adalimumab. Also, the levels of neonatal Fc receptor (FcRn) and FcRn mRNA were measured to explore the role of FcRn in the PK interaction between delanzomib and adalimumab. As a result, delanzomib combined with adalimumab exhibited stronger anti-arthritis activity than a single drug because both drugs synergistically reduced TNF-α level in vivo. Delanzomib also decreased adalimumab elimination in rats by increasing the level of FcRn. The slower elimination of adalimumab in rats further prolonged the anti-TNF-α effect of adalimumab. Moreover, FcRn level was increased by delanzomib via suppressing FcRn degradation rather than promoting FcRn production. In conclusion, delanzomib combined with adalimumab may be a potential therapeutic approach for treating rheumatoid arthritis. The initial finding that the PK interaction occurred between delanzomib and adalimumab may have clinical relevance for patients who simultaneously take proteasome inhibitors and anti-TNF-α therapeutic proteins.

scholarly journals Inflammatory and metabolic responses to high-fat meals with and without dairy products in men

2015 ◽  
Vol 113 (12) ◽  
pp. 1853-1861 ◽  
Author(s):  
Alexandra Schmid ◽  
Nicolai Petry ◽  
Barbara Walther ◽  
Ueli Bütikofer ◽  
Werner Luginbühl ◽  
...  
Keyword(s):  
Dairy Products ◽  
Plasma Concentrations ◽  
Hdl Cholesterol ◽  
Metabolic Responses ◽  
Low Grade ◽  
High Fat ◽  
Reactive Protein ◽  
Tnf Α ◽  
Postprandial Inflammation ◽  
Low Grade Inflammation

Postprandial inflammation is an important factor for human health since chronic low-grade inflammation is associated with chronic diseases. Dairy products have a weak but significant anti-inflammatory effect on postprandial inflammation. The objective of the present study was to compare the effect of a high-fat dairy meal (HFD meal), a high-fat non-dairy meal supplemented with milk (HFM meal) and a high-fat non-dairy control meal (HFC meal) on postprandial inflammatory and metabolic responses in healthy men. A cross-over study was conducted in nineteen male subjects. Blood samples were collected before and 1, 2, 4 and 6 h after consumption of the test meals. Plasma concentrations of insulin, glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol, TAG and C-reactive protein (CRP) were measured at each time point. IL-6, TNF-α and endotoxin concentrations were assessed at baseline and endpoint (6 h). Time-dependent curves of these metabolic parameters were plotted, and the net incremental AUC were found to be significantly higher for TAG and lower for CRP after consumption of the HFM meal compared with the HFD meal; however, the HFM and HFD meals were not different from the HFC meal. Alterations in IL-6, TNF-α and endotoxin concentrations were not significantly different between the test meals. The results suggest that full-fat milk and dairy products (cheese and butter) have no significant impact on the inflammatory response to a high-fat meal.

scholarly journals The Role of Oxidative Stress and Inflammation in Cardiovascular Aging

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Junzhen Wu ◽  
Shijin Xia ◽  
Bill Kalionis ◽  
Wenbin Wan ◽  
Tao Sun
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Low Grade ◽  
Oxygen Species ◽  
Age Related ◽  
Vascular Elasticity ◽  
Low Grade Inflammation

Age is an independent risk factor of cardiovascular disease, even in the absence of other traditional factors. Emerging evidence in experimental animal and human models has emphasized a central role for two main mechanisms of age-related cardiovascular disease: oxidative stress and inflammation. Excess reactive oxygen species (ROS) and superoxide generated by oxidative stress and low-grade inflammation accompanying aging recapitulate age-related cardiovascular dysfunction, that is, left ventricular hypertrophy, fibrosis, and diastolic dysfunction in the heart as well as endothelial dysfunction, reduced vascular elasticity, and increased vascular stiffness. We describe the signaling involved in these two main mechanisms that include the factors NF-κB, JunD, p66Shc, and Nrf2. Potential therapeutic strategies to improve the cardiovascular function with aging are discussed, with a focus on calorie restriction, SIRT1, and resveratrol.

scholarly journals Human Models of Low-Grade Inflammation: Bolus versus Continuous Infusion of Endotoxin

2007 ◽  
Vol 14 (3) ◽  
pp. 250-255 ◽  
Author(s):  
S. Taudorf ◽  
K. S. Krabbe ◽  
R. M. G. Berg ◽  
B. K. Pedersen ◽  
K. Møller
Keyword(s):  
Continuous Infusion ◽  
Inflammatory Mediators ◽  
Low Dose ◽  
Bolus Injection ◽  
In Vivo Model ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Endotoxin Infusion ◽  
Tnf Α ◽  
Low Grade Inflammation

ABSTRACT Systemic low-grade inflammation is recognized in an increasing number of chronic diseases. With the aim of establishing an experimental human in vivo model of systemic low-grade inflammation, we measured circulating inflammatory mediators after intravenous administration of Escherichia coli endotoxin (0.3 ng/kg of body weight) either as a bolus injection or as a 4-h continuous intravenous infusion, as well as after saline administration, in 10 healthy male subjects on three separate study days. Only bolus endotoxin caused an increase in heart rate, whereas a slight increase in rectal temperature was observed in both endotoxin groups. Tumor necrosis factor alpha (TNF-α), interleukin-6, and neutrophil responses were earlier and more pronounced in the bolus trial compared with the infusion trial results, whereas lymphocytes increased after endotoxin bolus injection as well as infusion without any difference between groups. Finally, endotoxin activated the hypothalamo-pituitary-adrenal axis slightly earlier in the bolus compared to the infusion trial. The continuous endotoxin infusion model may be more representative of human low-grade inflammation than the bolus injection model due to a less dynamic and more sustained increase in circulating levels of inflammatory mediators over time. In conclusion, low-dose endotoxin infusion elicits an inflammatory response, as assessed by a rise in TNF-α, and the responses are significantly different according to whether low-dose endotoxin is applied as a bolus injection or as a continuous infusion.

scholarly journals The effect of acute ophiobolin A treatment on HO-mediated inflammatory processes

2016 ◽  
Vol 36 (6) ◽  
pp. 594-602 ◽  
Author(s):  
Anikó Pósa ◽  
Renáta Szabó ◽  
Zita Szalai ◽  
Krisztina Kupai ◽  
Zoltán Deim ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Cardiac Tissue ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Inflammatory Processes ◽  
Factor Alpha ◽  
Fungal Secondary Metabolite ◽  
Inflammatory Molecules ◽  
Necrosis Factor

Many microbial and plant-derived metabolites contribute to the production of inflammatory mediators and the expression of pro-inflammatory molecules. Ophiobolin A (OPA) is a fungal secondary metabolite produced by Bipolaris species. The aim of our study was to examine the acute effects of this compound on inflammatory processes. Male Wistar rats were treated with 5% ethanol, 0.01 mg/kg OPA, 0.1 mg/kg OPA and 1.0 mg/kg OPA per os. After 24 h of the administrations, inflammatory mediators such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and myeloperoxidase (MPO) enzyme as well as heme oxygenase (HO) activity were measured in both plasma and cardiac tissue, along with serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). We found that OPA caused a significant elevation in the concentrations of IL-6 and TNF-α, increased MPO activity and decreased HO enzyme activity in the plasma. While OPA induces inflammation in the plasma, it did not change the level of inflammatory mediators in the cardiac tissue and the concentrations of serum ALT and AST. Our findings indicate that rapid release of inflammatory mediators by OPA promotes systemic inflammation. However, this acute OPA treatment does not show toxic effects on the cardiac tissue and the concentrations of liver enzymes.

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