scholarly journals Tomato-rich (Mediterranean) diet does not modify inflammatory markers

2007 ◽  
Vol 30 (2) ◽  
pp. 70 ◽  
Author(s):  
Arnon Blum ◽  
Merei Monir ◽  
Khalid Khazim ◽  
Aviva Peleg ◽  
Nava Blum
Keyword(s):  
Mediterranean Diet ◽  
Inflammatory Markers ◽  
Cardiovascular Events ◽  
Vascular Inflammation ◽  
Plasma Concentrations ◽  
Diet Group ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Markers Of Inflammation ◽  
Hs Crp

Background: The Mediterranean diet is rich in lycopene and has been reported to reduce cardiovascular events. The mechanism of prevention of cardiovascular events has not been clearly established. Our aim was to study the effects of a tomatoes-rich diet on markers of vascular inflammation. Methods: Plasma concentrations of E-selectin, intercellular adhesion molecule 1 (ICAM-1), and high sensitivity C-reactive protein (hs-CRP) were determined by ELISA in 103 apparently healthy volunteers. Volunteers were randomly assigned to two groups: 50 participants ate 300 g tomatoes daily for 1 month, and 53 participants ate their usual diet with tomatoes prohibited during that period. Markers of inflammation were measured before enrollment and 1 month after their assigned diet. Results: The two diet groups had similar baseline clinical characteristics and similar baseline levels of inflammatory markers. After 30 days of assigned diet concentrations of hs-CRP, E-selectin and ICAM-1 were unchanged compared with baseline in the tomato-rich diet. However, ICAM-1 concentraion was increased in the regular diet group from 247.55±55ng/ml to 264.71±60.42ng/ml (P=0.01). Conclusions: The mechanisms of benefit of the tomato-rich diet are not directly related to inhibition of markers of vascular inflammation.

scholarly journals Effects of Acute Fructose Loading on Markers of Inflammation—A Pilot Study

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3110
Author(s):  
Camilla Olofsson ◽  
Monica Eriksson ◽  
Ann-Christin Bragfors Helin ◽  
Björn Anderstam ◽  
Nicola Orsini ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Inflammatory Markers ◽  
Intercellular Adhesion Molecule ◽  
Low Grade ◽  
Intercellular Adhesion Molecule 1 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Postprandial State ◽  
Markers Of Inflammation ◽  
Bacterial Lipopolysaccharides ◽  
Cell Adhesion Molecule 1

Inflammation plays a role in development of diabetic complications. The postprandial state has been linked to chronic low grade inflammation. We therefore aimed to investigate the acute effects of fructose loading, with and without a pizza, on metabolic and inflammatory markers in patients with type 2 diabetes (T2D) (n = 7) and in healthy subjects (HS) (n = 6), age 47–76 years. Drinks consumed were blueberry drink (18 g fructose), Coca-Cola (17.5 g fructose), and fructose drink (35 g fructose). The levels of glucose, insulin, insulin-like growth factor binding protein-1 (IGFBP-1) and inflammatory markers: Interleukin-6 (IL-6), Monocyte chemoattractant protein-1 (MCP-1), Interleukin-18 (IL-18), Intercellular Adhesion Molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and bacterial lipopolysaccharides (LPS) were analyzed in blood. The postprandial responses were assessed using Wilcoxon’s matched-pairs test, Friedman’s ANOVA and Mann–Whitney U test. There was no difference in baseline levels of inflammatory markers between the groups. In T2D, MCP-1 decreased following blueberry drink and Coca-Cola (p = 0.02), Coca-Cola + pizza and fructose + pizza (p = 0.03). In HS, IL-6 increased following blueberry + pizza and fructose + pizza (p = 0.03), there was a decrease in MCP-1 following blueberry drink and Coca-Cola (p = 0.03), and in ICAM-1 following blueberry + pizza (p = 0.03). These results may indicate a role for MCP-1 as a link between postprandial state and diabetes complications, however further mechanistic studies on larger population of patients with T2D are needed for confirmation of these results.

scholarly journals Effects of oral and transdermal estrogen therapies on circulating cytokines and chemokines in postmenopausal women with hysterectomy

2009 ◽  
Vol 161 (2) ◽  
pp. 267-273 ◽  
Author(s):  
Toshiyuki Yasui ◽  
Ayako Saijo ◽  
Hirokazu Uemura ◽  
Toshiya Matsuzaki ◽  
Naoko Tsuchiya ◽  
...  
Keyword(s):  
Postmenopausal Women ◽  
Adhesion Molecule ◽  
Vascular Inflammation ◽  
Estrogen Therapy ◽  
Intercellular Adhesion Molecule ◽  
Serum Concentrations ◽  
Intercellular Adhesion Molecule 1 ◽  
Cytokines And Chemokines ◽  
Markers Of Inflammation ◽  
Circulating Levels

ObjectiveThe aim of the present study was to determine the different effects of oral estrogen therapy (ET) and transdermal ET on changes in circulating levels of cytokines and chemokines in relationship to changes in markers of inflammation in postmenopausal women with hysterectomy.MethodsFifty-five postmenopausal women with hysterectomy were randomly assigned in open, parallel-group fashion to an oral ET group and a transdermal ET group. Serum levels of cytokines and chemokines were simultaneously measured using a multiplexed human cytokine assay. Serum concentrations of high-sensitive C-reactive protein, soluble vascular cell adhesion molecule-1, soluble intercellular adhesion molecule-1, and E-selectin were measured as vascular inflammation markers.ResultsBoth oral ET and transdermal ET significantly decreased serum interleukin (IL)-7 concentrations at 12 months (P=0.020 and P=0.015 respectively). Transdermal ET decreased serum concentrations of IL-8, monocyte chemoattractant protein (MCP)-1, and macrophage inflammatory protein (MIP)-1β (P=0.05, P=0.019, and P=0.029), but oral ET increased IL-8 level (P=0.025). There were significant differences in percentage changes in IL-8 and MIP-1β between the oral and transdermal ET groups. Oral ET significantly decreased E-selectin level after 12 months.ConclusionTransdermal ET reduces circulating levels of IL-8, MCP-1, and MIP-1β, while both oral ET and transdermal ET reduce circulating level of IL-7.

scholarly journals Inhibition of PAR1 attenuates meningeal macrophage activation and vascular inflammation in a rat model of thrombin-induced hydrocephalus

2019 ◽  
Author(s):  
Xiaodi Hao ◽  
Xianghua Ye ◽  
Dan Shen ◽  
Chensheng Le ◽  
Lusha Tong ◽  
...  
Keyword(s):  
Subarachnoid Space ◽  
Vascular Inflammation ◽  
Intercellular Adhesion Molecule ◽  
Intraventricular Injection ◽  
Thrombin Injection ◽  
Intercellular Adhesion Molecule 1 ◽  
Neuron Loss ◽  
Meningeal Inflammation ◽  
M1 Polarization ◽  
Pro Inflammatory Cytokines

Abstract Background and Purpose— Our previous studies demonstrated that intraventricular injection of thrombin could induce hydrocephalus. The inflammation of subarachnoid space plays a key role in hydrocephalus. As thrombin, inducing coagulation, could contribute to inflammation, its effects on subarachnoid space have not been well studied. Macrophagic dysfunction may contribute to this course. However, the mechanisms that how thrombin affects macrophage in subarachnoid space have not been illustrated. Our aim was to explore the possible role that macrophage played in thrombin-induced meningeal inflammation, and to furtherly understand its contribution during thrombin-induced hydrocephalus. Methods— There were two parts in this study. Firstly, rats had an intraventricular injection of saline or thrombin. Secondly, rats received thrombin injection with vehicle or PAR1 antagonist treatment. Immunofluorescence staining was applied to observe the activation of meningeal macrophage and the expression of NeuN in the cortex. Meanwhile, the expression of intercellular adhesion molecule 1 (ICAM1) in meningeal vessels were tested to detect the vascular inflammation. Western blot was applied to measure the secretion of pro-inflammatory cytokines (IL-1β and IFNγ). Results— Our results demonstrated that intraventricular injection of thrombin caused significant activation of meningeal macrophages, vascular inflammation, and neuron loss. Inhibition of PAR1 pathway attenuated the M1 polarization of meningeal macrophage, reduced the inflammatory infiltrations and prevented the neuron loss, as well as hydrocephalus after thrombin injection. Conclusions— Clinically available PAR1 antagonists may offer a novel therapeutic approach candidate for the prevention or the management of inflammation in hemorrhage-induced hydrocephalus.

Skin cholesterol: test performance, evaluation of potential determinants and correlation analysis with cardiovascular risk factors and circulating markers of inflammation

VASA ◽  
2006 ◽  
Vol 35 (3) ◽  
pp. 167-173 ◽  
Author(s):  
Reiter ◽  
Wirth ◽  
Pourazim ◽  
Exner ◽  
Baghestanian ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Body Fat ◽  
Test Performance ◽  
Cardiovascular Events ◽  
Serum Lipids ◽  
Markers Of Inflammation ◽  
History Of ◽  
Hs Crp

Background: Skin cholesterol (SkC) has been suggested to be an additional risk predictor, so we evaluated the test performance, potential determinants of this marker as well as a potential correlation of SkC with markers of inflammation and the history of cardiovascular events. Patients and methods: SkC, determined by the non-invasive PREVU POC Skin Sterol test, as well as serum lipids, the body fat status, high-sensitive CRP (hs-CRP) and serum amyloid A (SAA) were evaluated in consecutive patients with and without documented atherosclerotic disease. Results: SkC was assessed in 201 patients. The within-day precision (CV) was 3.8%, the day-to-day CV of the right hand was 8.6% and 4.3% for the left hand, respectively. Neither univariate analysis nor multiple regressions identified a significant influence of age, sex, serum lipids, body fat status, smoking or diabetes mellitus on SkC, corresponding results were observed in a further analysis including 174 of these patients concerning hs-CRP and SAA (all p > 0.05). T-test analyses detected no significant differences between patients with and without a history of coronary, peripheral vascular and cerebrovascular events (all p > 0.05). Conclusions: The PREVU POC Skin Sterol test for the assessment of SkC proved an acceptable test performance. SkC is independent from serum lipids, traditional cardiovascular risk factors, two sensitive markers of systemic inflammation as well as the history of cardiovascular events indicating that the perception of this parameter as an established marker of vascular disease is premature.

Baseline ICAM-1 and VCAM-1 are Increased in Initially Healthy Middle-Aged Men who Develop Cardiovascular Disease during 6.6 Years of Follow-Up

Angiology ◽  
2008 ◽  
Vol 60 (1) ◽  
pp. 108-114 ◽  
Author(s):  
Caroline Schmidt ◽  
Johannes Hulthe ◽  
Björn Fagerberg
Keyword(s):  
Adhesion Molecule ◽  
Femoral Artery ◽  
Cardiovascular Events ◽  
High Serum ◽  
Intercellular Adhesion Molecule ◽  
Serum Concentrations ◽  
Intercellular Adhesion Molecule 1 ◽  
Baseline Serum ◽  
Increased Risk

The objective of the present study was to investigate if there was a difference in baseline serum concentrations of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) between groups with and without cardiovascular events during a mean follow-up of 6.6 years in a group of initially healthy 58-year-old men. A further aim was to examine if high serum concentrations of ICAM-1 and VCAM-1 were associated with carotid and femoral artery plaque occurrence, separately. Men with cardiovascular events during follow-up had higher median serum ICAM-I and VCAM-I than those without events ( P < .05). The median of serum ICAM-I and VCAM-1 in the event group was used as the cutoff level, and in those with ICAM-1 and VCAM-1 above the cutoff value, there was an increased risk of having a plaque in the femoral artery (OR = 2.8, 95% CI = 1.8-4.3; and OR = 1.6, 95% CI = 1.1-2.5, respectively).

Continuous therapy with transdermal nitroglycerin does not affect biomarkers of vascular inflammation and injury in healthy volunteers

2009 ◽  
Vol 87 (6) ◽  
pp. 455-459 ◽  
Author(s):  
George R. Thomas ◽  
Jonathan M. DiFabio ◽  
Tommaso Gori ◽  
David J.A. Jenkins ◽  
John D. Parker
Keyword(s):  
Healthy Volunteers ◽  
Vascular Inflammation ◽  
Venous Blood ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Continuous Exposure ◽  
Intercellular Adhesion Molecule 1 ◽  
Continuous Therapy ◽  
Factor Α ◽  
Dimethyl Arginine

Continuous exposure to nitroglycerin (GTN) results in development of tolerance and is associated with increased free radical production and abnormal endothelial function. Elevated plasma biomarkers of inflammation have been shown to be associated with endothelial dysfunction in most cardiovascular conditions. It remains unclear whether exposure to GTN is also associated with increased biomarkers of endothelial and vascular injury or vascular inflammation. In an investigator-blind study, a total of 28 healthy volunteers were randomized to continuous therapy with GTN (0.6 mg/h 24 h/day for 7 days) or no therapy. Venous blood was collected on day 0 and day 7. Plasma levels of markers such as asymmetric dimethyl-arginine (ADMA), human soluble P-selectin, interleukin-6, tumor necrosis factor-α, intercellular adhesion molecule-1, and oxidized low-density lipoproteins were measured. The levels of blood markers on day 0 were similar in the control and GTN-treated groups. After 7 days of GTN exposure, there were no significant changes in the different markers of vascular inflammation and injury either in the GTN or control group (all p > 0.5). The present study documents that prolonged continuous therapy with transdermal GTN therapy is not associated with changes in markers of vascular inflammation and injury.

Abstract 11678: Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Xinyuan Li ◽  
Pu Fang ◽  
Ya-Feng Li ◽  
Yin-Ming Kuo ◽  
Andrew J Andrews ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Activation ◽  
Nuclear Translocation ◽  
Fluorescence Probe ◽  
Vascular Inflammation ◽  
Intercellular Adhesion Molecule ◽  
Mitochondrial Calcium ◽  
Activator Protein 1 ◽  
Intercellular Adhesion Molecule 1 ◽  
Endothelial Cell Activation

Background: Lysophosphatidylcholines (LPCs) are a class of pro-inflammatory lipids that play important roles in atherogenesis. LPC activates endothelial cells (ECs) to upregulate adhesion molecules and chemokines, which is the initiation step of atherogenesis. However, the mechanisms underlying LPC-triggered EC activation are not fully understood. Previously considered as the toxic by-products of cellular metabolism, mitochondrial ROS (mtROS) are recently found to directly contribute to both the innate and adaptive immune responses. Here we tested a novel hypothesis that mtROS serve as signaling mediators for LPC-induced EC activation. Methods and Results: Using electron spin resonance and flow cytometry with fluorescence probe MitoSOX, we found that several LPC species including LPC 16:0, 18:0, and 18:1 induced mtROS in human primary aortic ECs (HAECs). Mechanistically, our analysis using mitochondrial calcium inhibitor and Seahorse XF96 mitochondrial function analyzer showed that LPC induced mtROS via increasing mitochondrial calcium entry which resulted in mitochondrial proton leakage. In addition, we found that mtROS scavenger MitoTEMPO abolished LPC-induced EC activation by downregulating Intercellular adhesion molecule 1 (ICAM-1) and Vascular cell adhesion protein 1 (VCAM-1) in HAECs. Moreover, our analysis with transcription factor profiling screening showed that MitoTEMPO acts by blocking LPC-induced nuclear translocation of pro-inflammatory transcription factor activator protein-1 (AP-1). Conclusions: Our results indicate that mtROS are responsible for LPC-induced EC activation and that mtROS may serve as a novel therapeutic target for vascular inflammation.

Inhibition of STAT3 phosphorylation by sulforaphane reduces adhesion molecule expression in vascular endothelial cell

2016 ◽  
Vol 94 (11) ◽  
pp. 1220-1226 ◽  
Author(s):  
Young S. Cho ◽  
Chan H. Kim ◽  
Tae S. Ha ◽  
Hee Y. Ahn
Keyword(s):  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Vascular Inflammation ◽  
Vascular Endothelial Cell ◽  
Vascular Wall ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Induced Expression ◽  
Stat3 Phosphorylation ◽  
Umbilical Vein Endothelial Cells

Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) play key roles in the initiation of vascular inflammation. In this study, we explored whether sulforaphane, a dietary phytochemical, can inhibit the expression of ICAM-1 and VCAM-1 in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS), and the mechanisms involved. Sulforaphane prevented the LPS-mediated increase in ICAM-1 and VCAM-1 expression, (P < 0.01) in HUVEC. Sulforaphane also prevented the LPS-mediated increase in the phosphorylation of signal transducer and activator of transcription 3 (STAT3) (P < 0.01). Stattic, a STAT3 inhibitor, reduced the LPS-induced expression of ICAM-1 and VCAM-1, and STAT3 phosphorylation (P < 0.01). STAT3 small interfering RNA treatment reduced the LPS-induced expression of ICAM-1, VCAM-1, and STAT3 (P < 0.01). Sulforaphane reduced LPS-mediated THP-1 monocyte adhesion to HUVEC (P < 0.01). In C57BL/6 mice, injection of LPS increased aortic ICAM-1 and VCAM-1 expression, and this effect was prevented by sulforaphane. These data provide insight into the mechanism through which sulforaphane partly reduces the expression of ICAM-1 and VCAM-1 on the vascular wall by inhibiting STAT3 phosphorylation.

Sign in / Sign up

Export Citation Format

Share Document