scholarly journals Effect of genistein and daidzein on platelet aggregation and monocyte and endothelial function

2003 ◽  
Vol 89 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Nicole Gottstein ◽  
Benjamin A. Ewins ◽  
Clair Eccleston ◽  
Gary P. Hubbard ◽  
Ian C. Kavanagh ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
No Production ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Tnf Α ◽  
Artery Disease

There has been much recent interest in the cardiovascular benefits of dietary isoflavones. The aim of the presentin vitrostudies was to investigate potential anti-thrombogenic and anti-atherogenic effects of the isoflavones genistein and daidzein in platelets, macrophages and endothelial cells. Pre-treatment with either isoflavone inhibited collagen-induced platelet aggregation in a dose-dependent manner. In a macrophage cell line (RAW 264·7) activated with interferon γ plus lipopolysaccharide, both isoflavones were found to inhibit NO production and tumour necrosis factor α (TNF-α) secretion dose-dependently, but they did not affect mRNA levels for inducible nitric oxide synthase and cyclo-oxygenase-2. Both isoflavones also dose-dependently decreased monocyte chemoattractant protein-1 secretion induced by TNF-α in human umbilical vein endothelial cells. Compared with daidzein, genistein exerted greater inhibitory effects for all parameters studied. The present data contributes to our knowledge on the molecular mechanisms by which isoflavones may protect against coronary artery disease. Further studies are required to determine whether the effects of isoflavones observed in the currentin vitrostudies are relevant to the aetiology of coronary artery diseasein vivo.

Abstract 20478: Circulating Inflammatory Potential Measured by an Endothelial Biosensor Assay in Coronary Artery Disease Patients

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Heidi Cung ◽  
Joe Anderson ◽  
James Nawarskas ◽  
Matthew Campen
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Adhesion Molecule ◽  
Inflammatory Markers ◽  
Serum Samples ◽  
Control Subjects ◽  
Tnf Α ◽  
Healthy Control ◽  
Artery Disease

Introduction: Vascular disease is driven by systemic inflammation that can arise from sites distal to the affected coronary or cerebral vessels. The objective of this study is to characterize the inflammatory potential of serum from patients with coronary artery disease (CAD) using cultured endothelial cells as a biosensor of the circulating milieu. Methods: Serum samples from CAD patients (N=48) and healthy control subjects (N=50) were incubated with primary human coronary artery endothelial cells at a 1:10 dilution for 4h, following by isolation of the cellular RNA. Alteration of inflammation-responsive elements (adhesion molecules and cytokines) was assessed on a gene expression level. Specific indicators included intercellular adhesion molecule-1 (ICAM), vascular cell adhesion molecule-1 (VCAM), and interleukin-8 (IL-8). Additionally, the serum samples from the CAD patients and healthy individuals were quantitatively analyzed for IL-1β, IL-6, IL-8, and TNF-α using an electrochemical luminescence platform. Results: For the CAD subjects’ serum, the mean values of ICAM, VCAM, and IL-8 expression were all elevated compared to healthy control subjects (p<0.001 for each by Students T-test). Correlational analysis revealed the three indicators (ICAM, VCAM, and IL-8) to be independent of each other and also other inflammatory markers such as C-reactive protein. IL-8 expression was negatively correlated with serum HDL levels but positively correlated with body fat composition. Interestingly, serum levels of IL-1β, IL-6, IL-8, and TNF-α in CAD patients were not statistically different from healthy control subjects. Conclusions: As yet uncharacterized circulating factors in the serum of CAD patients appear to activate endothelial cells. This assay paradigm performed well in terms of discriminating patients with CAD compared to healthy subjects, with greater range and specificity than specific inflammatory markers.

Opium may affect coronary artery disease by inducing inflammation but not through the expression of CD9, CD36, and CD68

2021 ◽  
pp. jim-2021-001935
Author(s):  
Mohammad Amin Momeni-Moghaddam ◽  
Gholamreza Asadikaram ◽  
Mohammad Masoumi ◽  
Erfan Sadeghi ◽  
Hamed Akbari ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Mrna Levels ◽  
Tnf Α ◽  
Opium Addiction ◽  
Ifn Γ ◽  
Artery Disease

The molecular mechanisms of opium with regard to coronary artery disease (CAD) have not yet been determined. The aim of the present study was to evaluate the effect of opium on the expression of scavenger receptors including CD36, CD68, and CD9 tetraspanin in monocytes and the plasma levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx) in patients with CAD with and without opium addiction. This case–control study was conducted in three groups: (1) opium-addicted patients with CAD (CAD+OA, n=30); (2) patients with CAD with no opium addiction (CAD, n=30); and (3) individuals without CAD and opium addiction as the control group (Ctrl, n=17). Protein and messenger RNA (mRNA) levels of CD9, CD36, and CD68 were evaluated by flow cytometry and reverse transcription-quantitative PCR methods, respectively. Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group. The plasma level of TNF-α was significantly higher in the CAD+OA group than in the CAD and Ctrl groups (p=0.001 and p=0.005, respectively). MDA levels significantly increased in the CAD and CAD+OA groups in comparison with the Ctrl group (p=0.010 and p=0.002, respectively). No significant differences were found in CD9, CD36, CD68, IFN-γ, and NOx between the three groups. The findings demonstrated that opium did not have a significant effect on the expression of CD36, CD68, and CD9 at the gene and protein levels, but it might be involved in the development of CAD by inducing inflammation through other mechanisms.

scholarly journals In Vitro Antiatherothrombotic Effects of Extracts from Berberis Vulgaris L., Teucrium Polium L., and Orthosiphon Stamineus Benth

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Nurul Huda Mohd Nor ◽  
Fauziah Othman ◽  
Eusni Rahayu Mohd Tohit ◽  
Sabariah Md Noor ◽  
Rosniza Razali ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Aqueous Extract ◽  
Antiplatelet Activity ◽  
Orthosiphon Stamineus ◽  
Berberis Vulgaris ◽  
Teucrium Polium ◽  
Artery Disease

Coronary artery disease is the leading cause of mortality and morbidity worldwide. The pathogenesis is mainly due to atherosclerosis, plaque rupture, and platelet thrombus formation. The main risk factors for coronary artery disease include obesity, hypercholesterolemia, smoking, diabetes, and high blood pressure. As a part of disease management, treatment options using anticoagulant and antiplatelet drugs can be applied with addition to lipid-lowering medication. However, medicinal plants comprising antiatherothrombotic effects can be used as options to combat the disease rather than drug therapies with lesser adverse effects. Therefore, the haematological effect of Berberis vulgaris L., Teucrium polium L., and Orthosiphon stamineus Benth extracts was studied using in vitro model to prevent and to treat coronary atherothrombotic disease. The aqueous, methanol, and polysaccharide extracts of B. vulgaris, T. polium, and O. stamineus, respectively, were studied for their anticoagulant and antiplatelet effect on human whole blood. Extracts were subjected to the prothrombin time (PT) and activated partial thromboplastin time (APTT) test for anticoagulant activity. The antiplatelet activity was investigated using an electrical impedance method. B. vulgaris aqueous extract (BVAE), B. vulgaris polysaccharide extract (BVPE), T. polium aqueous extract (TPAE), and T. polium polysaccharide extract (TPPE) significantly prolonged the coagulation time in a concentration-dependent manner (p<0.05). The administration of BVAE demonstrated the most effective antiplatelet activity against platelet aggregation caused by arachidonic acid (AA) and collagen. These antiplatelet activities may correspond to the presence of higher total phenolic compound, which thus inhibit the platelet aggregation activity. In conclusion, these findings provide strong evidence on the antiatherothrombotic effect of BVAE and TPAE.

scholarly journals The clinical impact of serum sLOX-1 level in coronary artery disease patients as inferred from its implication in the in vitro protective effects of metoprolol against hypoxic injury of HUVECs

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M.S Ali Sheikh ◽  
A Alduraywish ◽  
A Almaeen ◽  
U Salma ◽  
L Fei ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Protective Effect ◽  
Serum Levels ◽  
Hypoxic Injury ◽  
Injury Model ◽  
Artery Disease ◽  
Healthy Participants

Abstract Background Ischemic coronary artery disease (CAD) is a major public health problem across the world. Early detection and appropriate management significantly reduced CAD-induced morbidities and death. Endothelial cells are pathogenically implicated. Purpose Our study was designed to investigate the role of the soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) in the in vitro protective effect of Metoprolol against hypoxia-induced injury of Human umbilical vein endothelial cells (HUVECs). Secondly, the clinical significance of variations in serum levels of sLOX-1 in patients with CAD was assessed. Methods In vitro, hypoxic injury model of HUVECs was established in an atmosphere of 1% O2, 95% N2, and 5% CO2 for 24 hours. The protective effect and mechanism of action of the cardio-selective beta-blocker Metoprolol at 10–6 μM concentration was investigated. Consented stable atherosclerotic CAD (n=150) and unstable angina pectoris patients (n=75) along with 150 healthy volunteer subjects were voluntarily enrolled in this ethically approved study. Invasive coronary angiogram with ≥50% stenosis at least in one major coronary artery was used for diagnosis. ESC/ACC/AHC/practical protocols were used for categorizing patients into stable or unstable CAD. Serum sLOX-1 level was measured using specific ELISA kit. The diagnostic significance of serum sLOX-1 levels was assessed by analyzing its area under the curve (AUC). Results In vitro hypoxic conditions induced high rate of cellular apoptosis, high levels of LOX-1 expression, reactive oxygen species (ROS) generation and LDH release from HUVECs after 24 hours incubation, compared to normoxic control cells. Metoprolol significantly decreased LOX-1 levels, and prevented the release of LDH and generation of ROS. This culminated into marked improvement in cellular viability of hypoxia-exposed HUVECs (p&lt;0.001). Compared to healthy subjects, serum levels of sLOX-1s were significantly elevated in atherosclerotic stable and unstable CAD patients (p&lt;0.001). Serum sLOX-1 levels were increased by 4.21 folds in stable CAD patients and by 6.373 folds in atherosclerotic unstable angina patients vs. healthy participants. Moreover, the levels in the two patients' groups were significantly different (p&lt;0.001). In stable angina CAD patients, sLOX-1 AUC = 0.929; and in unstable CAD patients, AUC = 0.944, indicating that serum sLOX-1 levels clearly differentiated patients from healthy participants with high specificity and sensitivity. Conclusions Extrapolated from HUVECs hypoxia-induced injury model and the protective effect of Metoprolol, elevation of the circulating levels of sLOX-1 correlated with increased risks for atherosclerotic CAD and is a highly sensitive and specific biomarker for early detection of the disease. Funding Acknowledgement Type of funding source: None

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

Thrombopoietin and platelet aggregation in patients with stable coronary artery disease

Platelets ◽  
2017 ◽  
Vol 28 (8) ◽  
pp. 822-824
Author(s):  
Sanne Bøjet Larsen ◽  
Erik Lerkevang Grove ◽  
Søs Neergaard-Petersen ◽  
Morten Würtz ◽  
Anne-Mette Hvas ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

Monocyte-derived dendritic cells of patients with coronary artery disease show an increased expression of costimulatory molecules CD40, CD80 and CD86 in vitro

2007 ◽  
Vol 18 (7) ◽  
pp. 523-531 ◽  
Author(s):  
Jörn F. Dopheide ◽  
Urban Sester ◽  
Axel Schlitt ◽  
Georg Horstick ◽  
Hans J. Rupprecht ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Dendritic Cells ◽  
Coronary Artery ◽  
Costimulatory Molecules ◽  
Artery Disease

scholarly journals Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea

2021 ◽  
Vol 10 (15) ◽  
pp. 3413
Author(s):  
Afrouz Behboudi ◽  
Tilia Thelander ◽  
Duygu Yazici ◽  
Yeliz Celik ◽  
Tülay Yucel-Lindberg ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Obstructive Sleep Apnea ◽  
Coronary Artery ◽  
Sleep Apnea ◽  
Gene Polymorphism ◽  
Excessive Daytime Sleepiness ◽  
Daytime Sleepiness ◽  
Obstructive Sleep ◽  
Tnf Α ◽  
Artery Disease

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

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