Aronia juice consumption prior to half-marathon race can acutely affect platelet activation in recreational runners

Long-distance running, especially in non-professional runners, can increase cardiac arrest risk by enhancing platelet activation and aggregation. Polyphenols can exert cardioprotective effects by positively influencing platelet function. This study aimed to examine the acute effects of polyphenol-rich aronia juice consumption, before simulation of a half-marathon race, on platelet activation and aggregation with leukocytes in recreational runners. In this acute crossover study,10 healthy male runners (age 30.8 ± 2.3 years) consumed breakfast with 200 mL of aronia juice or 200 mL of placebo. They warmed-up and ran a simulated half-marathon race (21.1 km). Blood was collected at baseline, and at 15 min, 1 h, and 24 h after the run. All variables were analyzed with 4 (time) × 2 (group) ANOVA with repeated measures on both factors. Results revealed a significant effect of group on platelet activation parameters: P-selectin and GPIIb-IIIa expressions significantly decreased in the aronia group compared with the placebo group (F[1,9] = 10.282, p = 0.011 and F[1,9] = 7.860, p = 0.021, respectively). The effect of time was significant on both platelet aggregation markers: platelet-monocyte and platelet-neutrophil aggregates were significantly lower after the race (F[3,7] = 4.227, p = 0.014 and F[3,7] = 70.065, p = 0.000, respectively), with changes more pronounced in the later. All effects remained when platelets were exposed to an agonist. These results suggest that aronia consumption could counteract the half-marathon race-induced changes in platelet function. Novelty Aronia juice consumption significantly decreased the expression of platelet activation markers but did not affect platelet aggregation. The race itself did significantly reduce platelet-neutrophil aggregation. Aronia juice may serve as a supplement beverage for recreational runners to alleviate enhanced platelet reactivity caused by prolonged running.

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Dabigatran Treatment Increased Closure Device-Related Thrombosis by Platelet Activation in Patients Undergoing Percutaneous Left Atrial Appendage Closure

10.21203/rs.3.rs-346548/v1 ◽

2021 ◽

Author(s):

Xiaoye Li ◽

Xiaochun Zhang ◽

Qinchun Jin ◽

Yanli Li ◽

Junbo Ge ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Plasma Levels ◽

Multivariate Regression ◽

Left Atrial Appendage ◽

Platelet Reactivity ◽

Closure Device ◽

Activation Markers ◽

Significant Difference ◽

Operation Procedure

Abstract Background This study was designed to evaluate the platelet reactivity of different antithrombotic regimens under the condition of occluder implantation. Methods A single, prospective cohort study was conducted among patients who received anticoagulation with either dabigatran (N = 33) or rivaroxaban (N = 72) between January 2018 and December 2019. We applied thromboelastogram (TEG) to evaluate platelet aggregation induced with thrombin receptor activating peptide (TRAP) after anticoagulation for 3 months. Plasma coagulation markers mediate platelet activation including TAT, P-selectin, vWF and CD40L were tested by the method of ELISA kit on the day of LAAC and at 3 months after operation procedure. Repeated transesophageal echocardiographic were scheduled to evaluate device related thrombosis (DRT) formation on occluders at 3-month after discharge. Results There was 3(4.2%) in rivaroxaban and 4(12.1%) in dabigatran group experiencing DRT events (OR = 0.315, 95%CI:0.066–1.489, P = 0.129) during follow-ups. The TRAP induced platelet aggregation was higher for patients medication with dabigatran as compared to rivaroxaban group (62.9% vs. 59.7%, P = 0.028*). The plasma levels of TAT, P-selectin, vWF expression was significant higher after 3 months intake of dabigatran compared with that on the day LAAC operation, meanwhile, no significant difference was found in the changes of CD40L plasma levels. After receiving 3 months anticoagulation with rivaroxaban, the expressions of plasma platelet activation of TAT, P-selectin, vWF and CD40L showed no significant changes. We observed significant higher expressions of plasma platelet activation markers for DTR patients in terms of the P-selectin and vWF compared with non-DRT patients. Multivariate regression shwed that anticoagualtion regimen (P = 0.022; OR = 4.366, 95%CI: 0.434–10.839) was an independent predictor for DRT in patients after LAAC operation, while non of the plasma platelet activation included was associated with DRT. Conclusions By avoiding peri-procedure DRT occurrence, it is possible that dabigatran usage might even be reduced, as they had been shown to increase expressions of platelet reactivity.

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Enhancing Effect of Collagen Receptor Polymorphisms on In Vitro Platelet Reactivity to Aspirin in Healthy Subjects.

Blood ◽

10.1182/blood.v108.11.1099.1099 ◽

2006 ◽

Vol 108 (11) ◽

pp. 1099-1099 ◽

Cited By ~ 1

Author(s):

Miho Ushida ◽

Yumiko Matsubara ◽

Shinichi Takahashi ◽

Hiroaki Ishihara ◽

Toshiro Shibano ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Function ◽

Repeated Measures ◽

Platelet Reactivity ◽

Inhibitory Effect ◽

Antiplatelet Drug ◽

Platelet Response ◽

Individual Variations ◽

Collagen Receptor

Abstract [Background] Aspirin (ASA) is widely used as an antiplatelet drug, and a large number of clinical trials with ASA demonstrated significant efficacies for prevention and treatment of athrothrombosis. Recently, accumulating evidences indicated that there are inter-individual variations in the platelet response to ASA. The subpopulation, called ASA resistance, has the inability of response to ASA on ex vivo or in vitro platelet function tests and the poor clinical outcomes, although the mechanism underlying the variability is largely unknown. To date, genetic factors were showed to have an impact on platelet reactivity to ASA, and the inter-individual variations in platelet response to ASA was also reported to be associated with platelet sensitivity to collagen. In this study, the association between collagen-induced platelet aggregation (CIPA) and genetic polymorphisms of collagen receptors, glycoprotein (GP) Ia and GPVI, was analyzed using platelets treated by ASA (ASA +/−). We also investigated the effect of these polymorphisms on platelet thromboxane (TXB2) levels, closely related to the final stages of the arachidonate pathway inhibited by ASA. [Methods] We recruited genetically unrelated Japanese males (n=172) at their regular checkups. The mean age was 46.7±5.1 years. The subjects had no apparent hematologic or vascular disease and were not taking any medications that affect platelet function. Written informed consent was obtained from all study subjects. Platelet-rich plasma (PRP) sample was incubated with ASA [final concentration (fc) 10μM] or vehicle for 30 min at 24 degree Centigrade, and CIPA (fc 2μg/ml) test was performed on each PRP sample. Subsequently, platelet TXB2 levels were measured in the supernatant after centrifugation of each sample of CIPA test. Genotypes of the 807TC, Glu534Lys, Asn927Ser polymorphisms of GPIa and the Ser219Pro, Lys237Glu, Thr249Ala, Gln317Leu, His322Asn polymorphisms of GPVI were determined using the single-nucleotide primer extension-based method. [Results] To examine the sensitivity of platelets to ASA in vitro, we analyzed CIPA and platelet TXB2 levels in ASA(+/−). The maximum platelet aggregation and TXB2 levels in ASA(+) were significantly lower than those in ASA(−) (paired t-test, p<0.0001 and p<0.0001, respectively). Next, we investigated the association between the collagen receptor polymorphisms and the maximum platelet aggregation in ASA (+/−). For ASA(−), all genotypes of GPIa and GPVI were not associated with the maximum platelet aggregation. For ASA(+), subjects with 807TT/TC of GPIa had higher aggregation compared to those with 807CC(P=0.0135) whereas no association was observed between other polymorphisms and the maximum platelet aggregation. Moreover, repeated measures ANOVA showed that the difference in this inhibitory effect of ASA was significant between the 807TT/TC and 807CC genotypes (p=0.0253); the 807CC genotype has higher inhibitory effect of ASA. There was no association between platelet TXB2 levels and the GPIa and GPVI polymorphisms both in ASA(+) and ASA(−). [Conclusion] The 807CC genotype of GPIa polymorphism is associated with higher sensitivity to ASA in CIPA.

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Platelet Activation Markers in Patients with Peripheral Arterial Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665429 ◽

1997 ◽

Vol 78 (06) ◽

pp. 1434-1437 ◽

Cited By ~ 33

Author(s):

Paolo Gresele ◽

Mariella Catalano ◽

Carlo Giammarresi ◽

Raul Volpato ◽

Rosanna Termini ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Platelet Function ◽

Arterial Disease ◽

Platelet Function Test ◽

Activation Markers ◽

Significant Difference ◽

Peripheral Arterial

SummaryPeripheral vascular disease (PVD) is an indicator of diffuse atherosclerosis and is associated with a greatly increased incidence of coronary heart and cerebrovascular disease. Although several studies have assessed whether in vivo platelet activation takes place in patients with PVD, no data are available comparing different platelet function tests in this patient population.We have compared prospectively four tests for the measurement of in vivo platelet activation (plasma βTG, plasma PF4, intraplatelet (βTG and urinary excretion of 11-dehydro-TXB2) and one in vitro platelet function test (ADP-induced platelet aggregation) in 63 well-characterized patients with intermittent claudication and in 18 age- and sex- matched healthy volunteers.No statistically significant difference was found between patients and controls for plasma βTG (20.0 ± 11.8 vs. 18.8 ± 9.0 ng/ml, respectively), plasma PF4 (5.2 ± 2.9 vs. 6.3 ± 3.5 ng/ml), βTG/PF4 ratio (4.0 ± 2.9 vs. 3.6 ± 1.8), intraplatelet pTG (4503 ± 1482 vs. 4059 ± 1065 ng/ml), and threshold aggregatory concentration of ADP (1.7 ± 0.72 vs. 1.45 ± 0.56 μM).Urinary 11-dehydro-TXB2 was instead significantly higher in the PVD group (55.4 ± 27.5 vs. 26.7 ± 7.0 ng/h, p <0.001).Our study shows that urinary 11-dehydro-TXB2 is a more sensitive index of in vivo platelet activation than the measurement of either platelet specific proteins or of in vitro platelet aggregation in patients with PVD.

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Transferrin Saturation Inversely Correlates with Platelet Function

Thrombosis and Haemostasis ◽

10.1055/s-0039-1681061 ◽

2019 ◽

Vol 119 (05) ◽

pp. 766-778 ◽

Cited By ~ 3

Author(s):

Cristina Barale ◽

Rouslan Senkeev ◽

Franca Napoli ◽

Marco De Gobbi ◽

Angelo Guerrasio ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Function ◽

Cardiovascular Events ◽

Platelet Reactivity ◽

Platelet Rich Plasma ◽

Transferrin Saturation ◽

Mitogen Activated Protein Kinase ◽

Hfe Gene ◽

Activation Markers

Background The association between iron overload (IO) and risk of cardiovascular disease is controversial. Epidemiological studies have found a significant negative association of transferrin (Tf) saturation and cardiovascular events suggesting that higher body iron possibly confer a protective effect towards developing cardiovascular events. The biological mechanisms of this phenomenon are unknown. Objective This article investigates the role of IO on platelet reactivity. Materials and Methods This study was a prospective case–control study comparing 45 patients with IO, mostly characterized by the HFE gene mutations C282Y and/or H63D, with 32 healthy controls. We evaluated: (1) platelet aggregation in both platelet-rich plasma and whole blood, (2) platelet membrane expression of the activation marker CD62P, (3) activation of platelet signalling phosphoinositide 3-kinase /Akt and mitogen-activated protein kinase/extracellular signal-regulated kinases (Erk)-1/2 pathways, (4) a pattern of in vivo platelet activation markers, and (5) iron biomarker predictors of platelet reactivity. Results IO patients had significantly lower platelet aggregability, expression of CD62P and phosphorylation amounts of pAkt and pErk-2 in response to agonists. Furthermore, patients with higher Tf saturation levels were characterized by lower circulating levels of sCD40L, PDGF-BB and thromboxane B2. Platelet aggregation and activation parameters inversely correlated with Tf saturation and the stepwise multivariate regression analysis underlined the role of Tf saturation in predicting platelet reactivity. We also found that in vitro platelet exposure to diferric Tf, but not to iron-depleted TF, dose-dependently inhibited platelet function in all investigated subjects. Conclusion Tf saturation is inversely associated with platelet reactivity and this could explain, at least in part, the association of high Tf and lower risk of cardiovascular diseases in IO.

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The Effect of Heparin vs. Citrate on the Interaction of Platelets with Vascular Graft Materials

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660145 ◽

1985 ◽

Vol 54 (04) ◽

pp. 842-848 ◽

Cited By ~ 14

Author(s):

Kandice Kottke-Marchant ◽

James M Anderson ◽

Albert Rabinovitch ◽

Richard A Huskey ◽

Roger Herzig

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Vascular Graft ◽

Time Course ◽

Platelet Reactivity ◽

Polymer Surfaces ◽

In Vitro Perfusion ◽

Citrate Anticoagulation ◽

Platelet Release

SummaryHeparin is known to affect platelet function in vitro, but little is known about the effect of heparin on the interaction of platelets with polymer surfaces in general, and vascular graft materials in particular. For this reason, the effect of heparin vs. citrate anticoagulation on the interaction of platelets with the vascular graft materials expanded polytetrafluoroethylene (ePTFE), Dacron Bionit (DB) and preclotted Dacron Bionit (DB/PC) was studied in a recirculating, in vitro perfusion system. Platelet activation, as shown by a decrease in platelet count, an increase in platelet release and a decrease in platelet aggregation, was observed for all vascular graft materials tested using heparin and was greater for Dacron and preclotted Dacron than for ePTFE. Significant differences between heparin and citrate anticoagulation were seen for platelet release, platelet aggregation and the relative ranking of material platelet-reactivity. However, the trends and time course of platelet activation were similar with both heparin and citrate for the materials tested.

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Effects of Ticlopidine of Platelet Function in Men with Stable Angina Pectoris

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660138 ◽

1985 ◽

Vol 54 (04) ◽

pp. 808-812 ◽

Cited By ~ 7

Author(s):

Ulf Berglund ◽

Henning von Schenck ◽

Lars Wallentin

Keyword(s):

Platelet Aggregation ◽

Angina Pectoris ◽

Platelet Function ◽

Plasma Levels ◽

Platelet Reactivity ◽

Inhibitory Effect ◽

Controlled Study ◽

Double Blind ◽

Platelet Factor

SummaryThe effects of ticlopidine (T) (500 mg daily) on platelet function were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. The in vitro platelet reactivity to aggregating agents, the platelet sensitivity to prostacyclin and the plasma levels of platelet specific proteins and fibrinogen were determined before and after 4 and 8 weeks of treatment. T exerted a potent inhibitory effect on ADP- and collagen-induced platelet aggregation. The effect of T was proportional to the pretreatment reactivity to ADP and collagen. The inhibitory effect of T on the epinephrine response was less pronounced. The plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen were not influenced by T. The platelet inhibition of prostacyclin was potentiated by T, and it was demonstrated that T and prostacyclin had synergistic inhibitory effects on platelet aggregation.

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microRNAs as Promising Biomarkers of Platelet Activity in Antiplatelet Therapy Monitoring

International Journal of Molecular Sciences ◽

10.3390/ijms21103477 ◽

2020 ◽

Vol 21 (10) ◽

pp. 3477

Author(s):

Teresa L. Krammer ◽

Manuel Mayr ◽

Matthias Hackl

Keyword(s):

Antiplatelet Therapy ◽

Platelet Activation ◽

Platelet Function ◽

Platelet Reactivity ◽

Therapy Monitoring ◽

Platelet Inhibition ◽

High Morbidity ◽

Platelet Function Tests ◽

Function Tests ◽

Plasma Mirna

Given the high morbidity and mortality of cardiovascular diseases (CVDs), novel biomarkers for platelet reactivity are urgently needed. Ischemic events in CVDs are causally linked to platelets, small anucleate cells important for hemostasis. The major side-effect of antiplatelet therapy are life-threatening bleeding events. Current platelet function tests are not sufficient in guiding treatment decisions. Platelets host a broad spectrum of microRNAs (miRNAs) and are a major source of cell-free miRNAs in the blood stream. Platelet-related miRNAs have been suggested as biomarkers of platelet activation and assessment of antiplatelet therapy responsiveness. Platelets release miRNAs upon activation, possibly leading to alterations of plasma miRNA levels in conjunction with CVD or inadequate platelet inhibition. Unlike current platelet function tests, which measure platelet activation ex vivo, signatures of platelet-related miRNAs potentially enable the assessment of in vivo platelet reactivity. Evidence suggests that some miRNAs are responsive to platelet inhibition, making them promising biomarker candidates. In this review, we explain the secretion of miRNAs upon platelet activation and discuss the potential use of platelet-related miRNAs as biomarkers for CVD and antiplatelet therapy monitoring, but also highlight remaining gaps in our knowledge and uncertainties regarding clinical utility. We also elaborate on technical issues and limitations concerning plasma miRNA quantification.

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Effect of alteplase on platelet function and receptor expression

Journal of International Medical Research ◽

10.1177/0300060519829991 ◽

2019 ◽

Vol 47 (4) ◽

pp. 1731-1739 ◽

Cited By ~ 1

Author(s):

Jun Lu ◽

Peng Hu ◽

Guangyu Wei ◽

Qi Luo ◽

Jianlin Qiao ◽

...

Keyword(s):

Arachidonic Acid ◽

Platelet Aggregation ◽

Platelet Activation ◽

Platelet Function ◽

Adenosine Diphosphate ◽

Receptor Expression ◽

Light Transmittance ◽

Dependent Manner ◽

Clot Retraction ◽

Platelet Receptors

Objective To investigate the role of alteplase, a widely-used thrombolytic drug, in platelet function. Methods Human platelets were incubated with different concentrations of alteplase followed by analysis of platelet aggregation in response to adenosine diphosphate (ADP), collagen, ristocetin, arachidonic acid or epinephrine using light transmittance aggregometry. Platelet activation and surface levels of platelet receptors GPIbα, GPVI and αIIbβ3 were analysed using flow cytometry. The effect of alteplase on clot retraction was also examined. Results This study demonstrated that alteplase significantly inhibited platelet aggregation in response to ADP, collagen and epinephrine in a dose-dependent manner, but it did not affect ristocetin- or arachidonic acid-induced platelet aggregation. Alteplase did not affect platelet activation as demonstrated by no differences in P-selectin levels and PAC-1 binding being observed in collagen-stimulated platelets after alteplase treatment compared with vehicle. There were no changes in the surface levels of the platelet receptors GPIbα, GPVI and αIIbβ3 in alteplase-treated platelets. Alteplase treatment reduced thrombin-mediated clot retraction. Conclusions Alteplase inhibits platelet aggregation and clot retraction without affecting platelet activation and surface receptor levels.

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The Endocannabinoid 2-Arachidonoylglycerol Regulates Platelet Function.

Blood ◽

10.1182/blood.v108.11.3904.3904 ◽

2006 ◽

Vol 108 (11) ◽

pp. 3904-3904

Author(s):

Samantha Baldassarri ◽

Alessandra Bertoni ◽

Paolo Lova ◽

Stefania Reineri ◽

Chiara Sarasso ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Platelet Function ◽

Cannabinoid Receptors ◽

Thromboxane A2 ◽

Human Platelets ◽

Dependent Manner ◽

Cb2 Receptor ◽

Thromboxane A2 Receptor

Abstract 2-Arachidonoylglycerol (2-AG) is a naturally occurring monoglyceride that activates cannabinoid receptors and meets several key requisites of an endogenous cannabinoid substance. It is present in the brain and hematopoietic cells, including macrophages, lymphocytes and platelets. 2-AG is released from cells in a stimulus-dependent manner and is rapidly eliminated by uptake into cells and enzymatic hydrolysis in arachidonic acid and glycerol. 2-AG might exert a very fine control on platelet function either through mechanisms intertwining with the signal transduction pathways used by platelet agonists or through mechanisms modulating specific receptors. The aim of this study was to define the role of 2-AG in human platelets and characterize the mechanisms by which it performs its action. Platelets from healthy donors were isolated from plasma by differential centrifugations and gel-filtration on Sepharose 2B. The samples were incubated with 2-AG (10–100 μM) under constant stirring in the presence or absence of various inhibitors. Platelet aggregation was measured by Born technique. We have found that stimulation of human platelets with 2-AG induced irreversible aggregation, which was significantly enhanced by co-stimulation with ADP (1–10 μM). Furthermore, 2-AG-dependent platelet aggregation was completely inhibited by ADP scavengers, aspirin, and Rho kinase inhibitor, as well as by antagonists of the 2-AG receptor (CB2), of the ADP P2Y12 receptor, and of the thromboxane A2 receptor. We further investigated the role of endocannabinoids on calcium mobilization. Intracellular [Ca2+] was measured using FURA-2-loaded platelets prewarmed at 37°C under gentle stirring in a spectrofluorimeter. 2-AG induced rapid increase of cytosolic [Ca2+] in a dose-dependent manner. This effect was partially blocked by ADP scavengers and CB2 receptor antagonists. Furthermore, 2-AG-induced [Ca2+] mobilization was totally suppressed by aspirin or the thromboxane A2 receptor antagonist. These results suggest that 2-AG is able to trigger platelet activation, and that this action is partially mediated by CB2 receptor and ADP. Furthmore, 2-AG-dependent platelet activation is totally dependent on thromboxane A2 generation.

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Anthocyanins Inhibit Platelet Activation and Attenuate Thrombus Growth In Both Human and Murine Thrombosis Models

Blood ◽

10.1182/blood.v116.21.3197.3197 ◽

2010 ◽

Vol 116 (21) ◽

pp. 3197-3197 ◽

Cited By ~ 2

Author(s):

Yan Yang ◽

Zhenyin Shi ◽

Adili Reheman ◽

Wuxun Jin ◽

Conglei Li ◽

...

Keyword(s):

Platelet Aggregation ◽

Platelet Activation ◽

Platelet Function ◽

Intravital Microscopy ◽

Platelet Adhesion ◽

Thrombus Formation ◽

Vessel Occlusion ◽

Shear Rates ◽

Perfusion Chamber ◽

Platelet Adhesion And Aggregation

Abstract Abstract 3197 Background: Thrombosis and cardiovascular diseases (CVDs) result from blood vessel occlusion by inappropriately activated platelets. They are the leading causes of morbidity and mortality worldwide. Anthocyanins are major phytochemicals abundant in plant food and have been shown to play a protective role against CVDs. Our previous studies have demonstrated that anthocyanins are antioxidative and prevent inflammation (J Biol Chem. 2005; 280:36792-01; Arterioscler Thromb Vasc Biol. 2007; 27:519-24), which may indirectly affect platelet function. It has also been reported that anthocyanins affect platelet activities in whole blood and platelet rich plasma (PRP). However, the direct effects of anthocyanins on platelet function and thrombus formation have not been studied. Methods: Here we investigated the effects of anthocyanins on thrombosis using purified platelets as well as several thrombosis models in vitro and in vivo. Cyaniding-3-gulucoside (Cy-3-g) and delphinidin-3-glucoside (Dp-3-g), the two predominantly bioactive compounds of anthocyanin preparations, were prepared from Polyphenol AS Company in Norway. Purified gel-filtered platelets and PRP from healthy human volunteers and C57BL/6J mice were incubated at 37°C for 10 minutes with different concentrations (0.5μM, 5μM and 50μM) of Cy-3-g, Dp-3-g or PBS buffer as a control. Platelet aggregation was assessed by aggregometry using 5μM ADP, 10μg/ml collagen, or 100μM thrombin receptor activating peptide (TRAP; AYPGKF) as agonists. Platelet adhesion and aggregation were assessed in response to an immobilized collagen matrix in an ex vivo perfusion chamber at both high (1800 s-1) and low (600 s-1) shear rates. The expression of activated GPIIbIIIa was determined via PAC-1 monoclonal antibody in flow cytometry. Lastly, the effects of anthocyanins on thrombus formation in C57BL/6J mice were assessed using a FeCl3-induced intravital microscopy thrombosis model. Results: Both Cy-3-g and Dp-3-g significantly inhibited platelet aggregation induced by collagen and TRAP in gel-filtered platelets, and inhibited aggregation induced by ADP, TRAP and collagen in human and mouse PRP. These inhibitory functions were observed at Cy-3-g and Dp-3-g doses as low as 0.5μM. Cy-3-g and Dp-3-g also reduced the surface expression of activated GPIIbIIIa on resting human platelets in a dose-dependent manner. These compounds also markedly reduced platelet adhesion and aggregation in perfusion chamber assays at both low and high shear rates. Using intravital microscopy, we further demonstrated that Cy-3-g and Dp-3-g decreased platelet deposition, destabilized thrombi, and prolonged the time required for thrombus formation and vessel occlusion. Conclusions: our data clearly demonstrated for the first time that anthocyanin compounds directly inhibited platelet activation, adhesion and aggregation, as well as attenuated thrombus growth at both arterial and veinous shear stresses. These effects on platelets likely contribute to the protective effects of anthocyanins against thrombosis and CVDs. Disclosures: No relevant conflicts of interest to declare.

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