Anthocyanins from red cabbage extract — evidence of protective effects on blood platelets

2012 ◽  
Vol 7 (4) ◽  
pp. 655-663 ◽  
Author(s):  
Joanna Saluk ◽  
Michał Bijak ◽  
Joanna Kołodziejczyk-Czepas ◽  
Małgorzata Posmyk ◽  
Krystyna Janas ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Platelet Activation ◽  
Blood Platelets ◽  
Protective Effects ◽  
Platelet Activity ◽  
Red Cabbage ◽  
Arachidonate Cascade ◽  
Wide Range ◽  
Antioxidative Effects

AbstractRed cabbage belongs to cruciferous vegetables recognized as a rich source of anthocyanins. Anthocyanins have a wide range of therapeutic advantages without adverse effects, including cardiovascular protective properties. For development of cardiovascular diseases, platelet activation is crucial; therefore compounds which inhibit platelet activation are sought after. The anti-platelet activity of anthocyanins has only been described and is still unclear. In our study, the extract of anthocyanins, obtained from fresh leaves of red cabbage, was used in vitro to examine their antioxidative effects on platelets under oxidative stress conditions which are responsible for hyperactivity of these cells. The antiplatelet and antioxidative activities were determined by platelet aggregation and specific markers of the arachidonate cascade with O2−· generation, and oxidative changes (carbonyl groups and 3-nitrotyrosine). Extracts (5–15 μM) protected platelet proteins and lipids against oxidative damage, and diminished platelet activation. Anthocyanins from red cabbage provided beneficial anti-platelet effects and might help prevent cardiovascular diseases.

scholarly journals Preparations from Selected Cucurbit Vegetables as Antiplatelet Agents – An in Vitro Study

2021 ◽  
Author(s):  
Agata Rolnik ◽  
Bartosz Skalski ◽  
Anna Stochmal ◽  
Beata Olas
Keyword(s):  
Platelet Activation ◽  
Cucurbita Pepo ◽  
Thrombus Formation ◽  
Blood Platelets ◽  
In Vitro Study ◽  
Blood Platelet ◽  
Arachidonic Acid Metabolism ◽  
Platelet Activity ◽  
Activated Platelets

Abstract Increased blood platelet activation plays an important role in cardiovascular diseases (CVDs). Recent experiments indicate that certain fruits and vegetables, including onion, garlic, and beetroot, have anti-platelet potential and therefore may reduce the likelihood of CVDs. While vegetables from the Cucuritaceae family are known to exerting beneficial antioxidant and anti-inflammatory effects, their effects on blood platelet activation are poorly understood. Therefore, the aim of the present study was to determine the effect on platelet adhesion of preparations from selected cucurbits: pumpkin (Cucirbita pepo; fruit without seeds), zucchini (Cucurbita pepo convar. giromontina; fruit with seeds), cucumber (Cucumis sativus; fruit with seeds), white pattypan squash (Cucurbita pepo var. patisoniana; fruit without seeds) and yellow pattypan squash (Cucurbita pepo var. patisoniana, fruit without seeds). It also evaluates the activity of these preparations on enzymatic lipid peroxidation in thrombin-activated washed blood platelets by TBARS assay. The study also determines the anti-platelet and anticoagulant properties of these five cucurbit preparations in whole blood by flow cytometry and with the total thrombus-formation analysis system (T-TAS) and evaluates the cytotoxicity of the tested preparations against platelets based on LDH activity. The results indicate that the yellow Cucurbita pepo var. patisoniana preparation demonstrated stronger anti-platelet properties than the other tested preparations, reducing the adhesion of thrombin-activated platelets to collagen/fibrinogen, and inhibiting arachidonic acid metabolism and GPIIb/IIIa expression on 10 µM ADP-activated platelets. None of the preparations was found to cause platelet lysis. Our findings provide new information on the anti-platelet activity of the tested cucurbit preparations and their potential for treating CVDs associated with platelet hyperactivity.

Resveratrol and cardiac fibrosis prevention and treatment

2021 ◽  
Vol 22 ◽  
Author(s):  
Parinaz Zivarpour ◽  
Željko Reiner ◽  
Jamal Hallajzadeh ◽  
Liaosadat Mirsafaei
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiac Fibrosis ◽  
Therapeutic Potential ◽  
Developed Countries ◽  
Clinical Results ◽  
Matrix Proteins ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Laboratory Models

: Cardiovascular diseases are some of the major causes of morbidity and mortality in developed or developing countries but in developed countries as well. Cardiac fibrosis is one of the most often pathological changes of heart tissues. It occurs as a result of extracellular matrix proteins accumulation at myocardia. Cardiac fibrosis results in impaired cardiac systolic and diastolic functions and is associated with other effects. Therapies with medicines have not been sufficiently successful in treating chronic diseases such as CVD. Therefore, the interest for therapeutic potential of natural compounds and medicinal plants has increased. Plants such as grapes, berries and peanuts contain a polyphenolic compound called "resveratrol" which has been reported to have various therapeutic properties for a variety of diseases. Studies on laboratory models that show that resveratrol has beneficial effects on cardiovascular diseases including myocardial infarction, high blood pressure cardiomyopathy, thrombosis, cardiac fibrosis, and atherosclerosis. In vitro animal models using resveratrol indicated protective effects on the heart by neutralizing reactive oxygen species, preventing inflammation, increasing neoangiogenesis, dilating blood vessels, suppressing apoptosis and delaying atherosclerosis. In this review, we are presenting experimental and clinical results of studies concerning resveratrol effects on cardiac fibrosis as a CVD outcome in humans.

scholarly journals Short fungal fractions of β-1,3 glucans affect platelet activation

2016 ◽  
Vol 311 (3) ◽  
pp. H725-H734 ◽  
Author(s):  
Hélène Vancraeyneste ◽  
Rogatien Charlet ◽  
Yann Guerardel ◽  
Laura Choteau ◽  
Anne Bauters ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Atp Release ◽  
Human Platelets ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Platelet Activity ◽  
Concentration Dependent Manner ◽  
Wide Range ◽  
Invasive Infections ◽  
Life Threatening

Platelets are capable of binding, aggregating, and internalizing microorganisms, which enhances the elimination of pathogens from the blood. The yeast Candida albicans is a pathobiont causing life-threatening invasive infections. Its cell wall contains β-1,3 glucans that are known to trigger a wide range of host cell activities and to circulate during infection. We studied the effect of β-1,3 glucan fractions (BGFs) consisting of diglucosides (Glc2), tetraglucosides (Glc4), and pentaglucosides (Glc5) on human platelets, their mechanisms of action, and their possible impact on host defenses. The effect of BGFs on the coagulation process was determined by measuring thrombin generation. Platelets pretreated with BGFs were analyzed in terms of activation, receptor expression, aggregation, and adhesion to neutrophils and to C. albicans. The results show that BGFs affected the endogenous thrombin potential in a concentration-dependent manner. For platelet activation, BGFs at a low concentration (2 μmol/l) reduced ATP release and prevented the phosphorylation of protein kinase C. BGFs diminished the expression of P-selectin and the activation of αIIbβ3. BGFs decreased platelet aggregation and the interaction between thrombin-stimulated platelets and neutrophils, fibrinogen, and C. albicans. GLc5 decreased ATP release and TGF-β1 production in response to TLR4 upregulation in thrombin-stimulated platelets, but TLR4 blockage abolished the effect of BGFs on platelets. This study provides evidence that fungal pentaglucosides modulate platelet activity mediated via TLR4 stimulation and reduce platelet-neutrophil interaction.

scholarly journals Protective Activity of C-Geranylflavonoid Analogs from Paulownia tomentosa against DNA Damage in 137Cs Irradiated AHH-1Cells

2014 ◽  
Vol 9 (9) ◽  
pp. 1934578X1400900
Author(s):  
Hyung-In Moon ◽  
Min Ho Jeong ◽  
Wol Soon Jo
Keyword(s):  
Dna Damage ◽  
Protective Effects ◽  
Strand Breaks ◽  
Human Lymphoblastoid Cell ◽  
Wide Range ◽  
Radiation Induced ◽  
Anti Oxidant ◽  
Dna Strand ◽  
Cellular Dna

Radiotherapy is an important form of treatment for a wide range of cancers, but it can damage DNA and cause adverse effects. We investigated if the diplacone analogs of P. tomentosa were radio-protective in a human lymphoblastoid cell line (AHH-1). Four geranylated flavonoids, diplacone, 3′- O-methyl-5′-hydroxydiplacone, 3′- O-methyl-5′- O-methyldiplacone and 3′- O-methyldiplacol, were tested for their antioxidant and radio-protective effects. Diplacone analogs effectively scavenged free radicals and inhibited radiation-induced DNA strand breaks in vitro. They significantly decreased levels of reactive oxygen species and cellular DNA damage in 2 Gy-irradiated AHH-1 cells. Glutathione levels and superoxide dismutase activity in irradiated AHH-1 cells increased significantly after treatment with these analogs. The enhanced biological anti-oxidant activity and radioprotective activity of diplacone analogs maintained the survival of irradiated AHH-1 cells in a clonogenic assay. These data suggest that diplacone analogs may protect healthy tissue surrounding tumor cells during radiotherapy to ensure better control of radiotherapy and allow higher doses of radiotherapy to be employed.

scholarly journals Thrombospondin-1 promotes haemostasis through modulation of cAMP signalling in blood platelets.

Blood ◽  
2020 ◽  
Author(s):  
Ahmed Aburima ◽  
Martin Berger ◽  
Benjamin EJ Spurgeon ◽  
Beth A Webb ◽  
Katie S Wraith ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Blood Platelets ◽  
Camp Signaling ◽  
Camp Accumulation ◽  
In Vivo Models ◽  
Downstream Signaling ◽  
Thrombospondin 1 ◽  
Increased Sensitivity

Thrombospondin-1 (TSP-1) is released by platelets upon activation and can promote platelet activation, but its role in haemostasis in vivo is unclear. We show that TSP-1 is a critical mediator of haemostasis that promotes platelet activation by modulating inhibitory cAMP signaling. Genetic deletion of TSP-1 did not affect platelet activation in vitro, but in vivo models of haemostasis and thrombosis demonstrated that TSP-1 deficient mice had prolonged bleeding, defective thrombosis and increased sensitivity to the prostacyclin mimetic iloprost. Adoptive transfer of wild type (WT), but not TSP-1-/- platelets, ameliorated the thrombotic phenotype, suggesting a key role for platelet-derived TSP-1. In functional assays, TSP-1-deficient platelets showed an increased sensitivity to cAMP signaling, inhibition of platelet aggregation and arrest under flow by PGI2. Plasma swap experiments showed that plasma TSP-1 did not correct PGI2 hypersensitivity in TSP-1-/- platelets. By contrast, incubation of TSP-1-/- platelets with releasates from WT platelets or purified TSP-1, but not releasates from TSP-1-/- platelets, reduced the inhibitory effects of PGI2. Activation of WT platelets resulted in diminished cAMP accumulation and downstream signaling, which was associated with increased activity of the cAMP hydrolyzing enzyme phosphodiesterase 3A (PDE3A). PDE3A activity and cAMP accumulation were unaffected in platelets from TSP-1-/- mice. Platelets deficient in CD36, a TSP-1 receptor, showed increased sensitivity to PGI2/cAMP signaling and diminished PDE3A activity, which was unaffected by platelet-derived or purified TSP-1. This suggests that the release of TSP-1 regulates haemostasis in vivo through modulation of platelet cAMP signaling at sites of vascular injury.

scholarly journals Amyloid Beta: Multiple Mechanisms of Toxicity and Only Some Protective Effects?

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Paul Carrillo-Mora ◽  
Rogelio Luna ◽  
Laura Colín-Barenque
Keyword(s):  
Amyloid Beta ◽  
Protective Effects ◽  
Protective Mechanisms ◽  
Experimental Conditions ◽  
Mechanisms Of Toxicity ◽  
Mitochondrial Alterations ◽  
Physiological Properties ◽  
Wide Range

Amyloid beta (Aβ) is a peptide of 39–43 amino acids found in large amounts and forming deposits in the brain tissue of patients with Alzheimer’s disease (AD). For this reason, it has been implicated in the pathophysiology of damage observed in this type of dementia. However, the role of Aβin the pathophysiology of AD is not yet precisely understood. Aβhas been experimentally shown to have a wide range of toxic mechanismsin vivoandin vitro, such as excitotoxicity, mitochondrial alterations, synaptic dysfunction, altered calcium homeostasis, oxidative stress, and so forth. In contrast, Aβhas also shown some interesting neuroprotective and physiological properties under certain experimental conditions, suggesting that both physiological and pathological roles of Aβmay depend on several factors. In this paper, we reviewed both toxic and protective mechanisms of Aβto further explore what their potential roles could be in the pathophysiology of AD. The complete understanding of such apparently opposed effects will also be an important guide for the therapeutic efforts coming in the future.

Progressive Increase in Platelet Activation With Smoke Exposure: Human Subject and In-Vitro Studies

2007 ◽  
Author(s):  
Gaurav Girdhar ◽  
Sulan Xu ◽  
Jolyon Jesty ◽  
Danny Bluestein
Keyword(s):  
Cigarette Smoke ◽  
Platelet Activation ◽  
Human Subject ◽  
Prolonged Exposure ◽  
Human Subjects ◽  
Progressive Increase ◽  
In Vitro Studies ◽  
Protective Effects ◽  
Shs Exposure

Second hand cigarette smoke (SHS) is one of the major risk factors for cardiovascular disease (CVD) and has been shown to substantiate platelet activation and aggregation in several studies [1, 2]. Most of these studies, under chronic or acute exposure conditions or over prolonged exposure, do not represent the initiation of a disease state or hematological damage under normal levels of cigarette smoke. These above studies of platelet activation with SHS together with our previous in-vitro studies demonstrating cardio-protective effects of nicotine [3], have motivated the present investigation of physiological levels of SHS exposure on human subjects and within an in-vitro endothelial cell-platelet system, with cigarettes (or smoke extracts) of varying nicotine content to confirm analogous cardio-protective effects of nicotine.

scholarly journals Increased Pro-Thrombotic Platelet Activity Associated with Thrombin/PAR1-Dependent Pathway Disorder in Patients with Secondary Progressive Multiple Sclerosis

2020 ◽  
Vol 21 (20) ◽  
pp. 7722
Author(s):  
Angela Dziedzic ◽  
Elzbieta Miller ◽  
Michal Bijak ◽  
Lukasz Przyslo ◽  
Joanna Saluk-Bijak
Keyword(s):  
Multiple Sclerosis ◽  
Mrna Expression ◽  
Platelet Activation ◽  
Blood Platelets ◽  
Surface Expression ◽  
Epidemiological Studies ◽  
Progressive Multiple Sclerosis ◽  
Apolipoprotein A1 ◽  
Platelet Activity ◽  
Activation Markers

Epidemiological studies confirm the high risk of ischemic events in multiple sclerosis (MS) that are associated with increased pro-thrombotic activity of blood platelets. The most potent physiological platelet agonist is thrombin, which activates platelets via cleavage of specific protease-activated receptors (PARs). Our current study is aimed to determine the potential genetics and proteomic abnormalities of PAR1 in both platelets and megakaryocytes, which may have thromboembolic consequences in the course of MS. The obtained results were correlated with the expression level of platelet and megakaryocyte transcripts for APOA1 and A2M genes encoding atherosclerosis biomarkers: apolipoprotein A1 (ApoA1) and α-2-macroglobulin (α2M), respectively. Moreover, PAR1 functionality in MS platelets was assessed by flow cytometry, determining the level of platelet–platelet and platelet–leukocyte aggregates, platelet microparticles and surface expression of P-selectin. As a PAR1 agonist, the synthetic TRAP-6 peptide was used, which made it possible to achieve platelet activation in whole blood without triggering clotting. Comparative analyses showed an elevated level of platelet activation markers in the blood of MS patients compared to controls. The mRNA expression of gene coding α2M was upregulated, whilst ApoA1 was down-regulated, both in platelets and megakaryocytes from MS patients. Furthermore, we observed an increase in both mRNA expression and surface density of PAR1 in platelets and megakaryocytes in MS compared to controls. Both the level of platelet activation markers and PAR1 expression showed a high correlation with the expression of transcripts for APOA1 and A2M genes.

IWR-1 Inhibits Collagen-Induced Platelet Activation and Protects against Thrombogenesis

2019 ◽  
Vol 39 (04) ◽  
pp. 392-397
Author(s):  
Wei Wang ◽  
Songqing Lai ◽  
ZiJin Xiao ◽  
Haiyue Yan ◽  
Yongxi Li ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Antiplatelet Agent ◽  
Wnt Signalling ◽  
In Vivo Studies ◽  
Dependent Manner ◽  
Platelet Activity ◽  
Occlusion Time ◽  
Negative Effect

AbstractPlatelets play a crucial role in haemostasis and several pathophysiological processes. Collagen is a main initiator for platelet activation and aggregation. Given that Wnt signalling negatively regulates platelet function, and IWR-1 (a small molecule inhibitor for Wnt signalling) has the potential of inhibiting collagen synthesis, it is essential to investigate whether IWR-1 regulates collagen-induced platelet activation and protects against thrombogenesis. In the present study we found that IWR-1 pretreatment effectively suppressed collagen-induced platelet aggregation in a dose-dependent manner. In addition, IWR-1 also resulted in a decrease of P-selectin and phosphatidylserine surface exposure using fluorescence-activated cell sorting analysis. In vitro studies further revealed that IWR-1 had a negative effect on integrin a2β1 activation and platelet spreading. More importantly, the results from in vivo studies showed that IWR-1 exhibited a robust bleeding diathesis in the tail-bleeding assay and a prolonged occlusion time in the FeCl3-induced carotid injury model. Taken together, current results demonstrate that IWR-1 could effectively block collagen-induced platelet activity in vitro and in vivo, and suggest its candidacy as a new antiplatelet agent.

Platelet Activation and Free Emboli Formation in Flow Past Mechanical Heart Valves

2002 ◽  
Author(s):  
Danny Bluestein ◽  
Wei Yin ◽  
Jolyon Jesty ◽  
Adam E. Saltman ◽  
Irvin B. Krukenkamp ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Heart Valves ◽  
Left Ventricular ◽  
Mechanical Heart Valves ◽  
Shear Stresses ◽  
Platelet Activity ◽  
Flow Past ◽  
Activity State ◽  
Valve Implantation

Numerical studies, in vitro, and in vivo measurements were conducted, aimed at quantifying free emboli formation and procoagulant properties of platelets induced by flow past mechanical heart valves (MHV). Pulsatile turbulent flow simulation was conducted past a St. Jude medical MHV in the aortic position, to study the effects of valve implantation technique on the thromboembolic potential of the valve. A misaligned valve with subannualarly sutured pledgets produced accelerating jet flow through the valve orifices and a wider wake of shed vortices. Shear stress histories of platelets along turbulent trajectories exposed the platelets to elevated shear stresses around the leaflets, leading them to entrapment within the shed vortices. In vitro platelet studies were conducted past the MHV mounted in a recirculation flow loop and in a model of left ventricular assist device (LVAD), using an innovative platelet activity state (PAS) assay. The platelet activation significantly increased as a function of the recirculation time past the valve, and as compared to controls. Transcranial Doppler (TCD) measurements were conducted in the carotid artery of sheep with implanted MHV, showing marked increase in the number of HITS (High Intensity Transient Signals) signifying the passage of free emboli generated by the valve. The HITS were analyzed to distinguish between gaseous and thrombi emboli. Finally, platelet activity state measurements were conducted with sheep platelets, showing marked increase of platelet activation after valve implantation.

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