Inhibitory Effect of 20(S)-Ginsenoside Rg3 on Human Platelet Aggregation and Intracellular Ca2+ Levels via Cyclic Adenosine Monophosphate Dependent Manner

Background Although halothane directly inhibits platelet aggregation, the mechanisms of this effect are still unknown. The current study aimed to clarify the inhibitory mechanisms of halothane on thrombin-induced human platelet aggregation by measuring (1) platelet-surface glycoprotein Ib expression, (2) the concentration of intracellular free Ca2+ ([Ca2+]i) measured simultaneously with aggregation, (3) the concentration of intracellular inositol 1,4,5-triphosphate, and (4) the concentration of intracellular cyclic 3',5'-adenosine monophosphate ([cAMP]i). Methods Washed platelet suspensions, obtained from healthy volunteers, were preincubated with halothane (0-2 mM) for 2 min and then exposed to 0.02 units/ml thrombin for 3 min. The glycoprotein Ib bound to fluorescein-labeled antibody was measured by fluorescence flow cytometry. [Ca2+]i was measured, simultaneously with aggregation, in Fura-2 (Ca2+ indicator)-loaded platelets by use of a fluorometer. Inositol 1,4,5-triphosphate and [cAMP]i were measured by radioimmunoassay. Results Halothane had no effect on glycoprotein Ib expression with or without thrombin. Halothane decreased the thrombin stimulated [Ca2+]i transient and inhibited platelet aggregation in a dose-dependent manner, both in the presence and in the absence of external Ca2+. Isoflurane had no apparent effect on either platelet aggregation or [Ca2+]i in the absence of external Ca2+. Halothane inhibited the increase in inositol 1,4,5-triphosphate induced by thrombin. Halothane moderately but significantly increased [cAMP]i, but the adenylate cyclase activator forskolin (which has the same inhibitory ability on aggregation as halothane) increased [cAMP]i to a much greater extent than did halothane. Conclusions Halothane inhibits thrombin-induced human platelet aggregation by decreasing [Ca2+]i without inhibiting agonist-receptor binding; the inhibitory effect of halothane on [Ca2+]i might be mediated by a decrease in inositol 1,4,5 triphosphate and in part by an increase in [cAMP]i.

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Inhibitory Effect of Staphylokinase on Platelet Aggregation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649679 ◽

1993 ◽

Vol 70 (05) ◽

pp. 834-837 ◽

Cited By ~ 6

Author(s):

Akira Suehiro ◽

Yoshio Oura ◽

Motoo Ueda ◽

Eizo Kakishita

Keyword(s):

Platelet Aggregation ◽

Human Platelet ◽

Degradation Products ◽

Platelet Rich Plasma ◽

Inhibitory Effect ◽

Effective Concentration ◽

Inhibit Platelet Aggregation ◽

Platelet Suspension ◽

Washed Platelet ◽

Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

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Heparin Counteracts the Antiaggregating Effect of Prostacyclin by Potentiating Platelet Aggregation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657326 ◽

1983 ◽

Vol 49 (02) ◽

pp. 081-083 ◽

Cited By ~ 13

Author(s):

Vittorio Bertelé ◽

Maria Carla Roncaglioni ◽

Maria Benedetta Donati ◽

Giovanni de Gaetano

Keyword(s):

Platelet Aggregation ◽

Human Platelet ◽

Specific Interaction ◽

Inhibitory Effect ◽

Effective Inhibitor ◽

Inhibitory Potency ◽

Human Platelet Aggregation

SummaryIt has recently been reported that heparin neutralizes the inhibitory effect of prostacyclin (PGI2) on human platelet aggregation. The mechanism of this interaction has not yet been unequivocally established. We present here evidence that heparin (Liquemin Roche) does not react directly with PGI2 but counteracts its inhibitory effect by potentiating platelet aggregation. In the absence of heparin, PGI2 was a less effective inhibitor of platelet aggregation induced by the combination of ADP and serotonin than by ADP alone. Moreover, the inhibitory effect of PGI2 was similarly reduced when increasing the concentrations of ADP (in the absence of heparin). The lack of a specific interaction between heparin and PGI2 is supported by the observation that, in the presence of heparin, other prostaglandins such as PGD2 and PGE1, and a non-prostanoid compound such as adenosine also appeared to lose their inhibitory potency. It is concluded that heparin opposes platelet aggregation inhibitory effect of PGI2 by enhancement of platelet aggregation.

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Inhibitory action of somatostatin-14 on hormone-stimulated cyclic adenosine monophosphate induction in porcine granulosa and luteal cells

Journal of Endocrinology ◽

10.1677/joe.0.1340297 ◽

1992 ◽

Vol 134 (2) ◽

pp. 297-306 ◽

Cited By ~ 12

Author(s):

K. Rajkumar ◽

D. E. Kerr ◽

R. N. Kirkwood ◽

B. Laarveld

Keyword(s):

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Inhibitory Effect ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Luteal Cells ◽

Camp Generation ◽

Camp Induction ◽

Camp Levels ◽

Somatostatin 14

ABSTRACT Somatostatin-14 (SRIF-14) inhibited, in a concentration-dependent manner, LH- and forskolin-stimulated cyclic adenosine monophosphate (cAMP) induction in porcine granulosa and luteal cells. The inhibitory effect of SRIF-14 on hormone-induced cAMP generation was more potent in porcine ovarian cells than in the GH-3 pituitary cell line. The inhibitory effect of SRIF-14 was impeded by neutralizing its biological activity with specific antiserum. Preincubation of luteal and granulosa cells with phorbol 12-myristate 13-acetate (PMA) enhanced LH- and forskolin-stimulated cAMP levels. SRIF-14 failed to inhibit LH- or forskolin-stimulated cAMP levels in cells preincubated with PMA. It is concluded that SRIF-14 inhibits hormone-stimulated cAMP induction in the porcine ovary. LH-induced protein kinase C activation may be physiologically important to alleviate the inhibitory effects of SRIF-14. Journal of Endocrinology (1992) 134, 297–306

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Potentiation of Adrenaline-Induced Platelet Aggregation by Angiotensin II

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660105 ◽

1985 ◽

Vol 54 (03) ◽

pp. 717-720 ◽

Cited By ~ 32

Author(s):

Yu-An Ding ◽

D Euan MacIntyre ◽

Christopher J Kenyon ◽

Peter F Semple

Keyword(s):

Platelet Aggregation ◽

Angiotensin Ii ◽

Human Platelet ◽

Inhibitory Effect ◽

Facilitatory Effect ◽

Ang Ii ◽

Human Platelet Aggregation ◽

Low Concentrations ◽

High Concentrations ◽

Stimulation Of

SummaryThe effects of angiotensin II (ANG II) alone and in combination with other agonists on human platelet aggregation, thromboxane B2 (TxB2) and cytosolic [Ca2+]i were investigated. ANG II (10™11 - 10™7 M) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (<2 min) or longterm (30 min) incubation. In contrast, low concentrations of ANG II (10™11 M) enhanced adrenaline-induced platelet aggregation but high concentrations (10™7 M) had an inhibitory effect. Moreover, ANG II (10™11 - 10™7 M) augmented platelet responses to the TxA2 mimetic, U44069. Pretreatment of platelets with flurbiprofen abolished this facilitatory effect of ANG II on adrenaline- but not on U44069-induced platelet aggregation. These results suggest that ANG II stimulation of agonist-induced platelet activation may be due to potentiation of the effects rather than the synthesis of TxA2

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Inhibitory Effect of Hexahydrocurcumin on Human Platelet Aggregation

Natural Product Communications ◽

10.1177/1934578x1200700719 ◽

2012 ◽

Vol 7 (7) ◽

pp. 1934578X1200700 ◽

Cited By ~ 3

Author(s):

Huei-Ping Dong ◽

Rei-Cheng Yang ◽

I-Chun Chunag ◽

Li-Ju Huang ◽

Hsing-Tan Li ◽

...

Keyword(s):

Platelet Aggregation ◽

Human Platelet ◽

Platelet Rich Plasma ◽

Adenosine Diphosphate ◽

Inhibitory Effect ◽

Human Platelet Aggregation

The effects of hexahydrocurcumin on adenosine diphosphate (ADP)-induced human platelet aggregation were studied. Treatment of human platelet-rich plasma with hexahydrocurcumin resulted in an inhibitory effect on platelet aggregation, suggesting the potential of this compound as an anti-atherosclerogenic agent in humans.

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Inhibitory effect of Ginkgo biloba extract on human platelet aggregation

Platelets ◽

10.1080/09537109975933 ◽

1999 ◽

Vol 10 (5) ◽

pp. 298-305 ◽

Cited By ~ 34

Author(s):

Asim K. Dutta-Roy, Margaret J. Gordon, C

Keyword(s):

Platelet Aggregation ◽

Ginkgo Biloba ◽

Human Platelet ◽

Inhibitory Effect ◽

Ginkgo Biloba Extract ◽

Human Platelet Aggregation

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Identification of Platelet Inhibitor Present in the Melon (Cucurbitacea Cucumis Melo)

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661304 ◽

1985 ◽

Vol 53 (03) ◽

pp. 312-313 ◽

Cited By ~ 9

Author(s):

Raul Altman ◽

Jorge Rouvier ◽

Hans Weisenberger

Keyword(s):

Platelet Aggregation ◽

Mass Spectroscopy ◽

Active Substance ◽

Cucumis Melo ◽

Human Platelet ◽

Inhibitory Effect ◽

Active Fraction ◽

Uv Spectrum ◽

Platelet Inhibitor ◽

Human Platelet Aggregation

SummaryAn active fraction was isolated from an aqueous melon extract (Cucurbitacea cucumis melo) and was shown that it inhibits human platelet aggregation induced by epinephrine, ADP, collagen, thrombin, sodium arachidonate, prostaglandin endoperoxide analogue U-46619 and PAF-acether. Identification of the active substance as adenosine was indicated by TLC which gave identical Rf value compared to adenosine, by the UV spectrum, because the inhibitory effect on platelet aggregation disappeared after the addition of adenosine-deaminase and because the substance under study and adenosine produced the same spectra in the mass spectroscopy.

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Differential Effect of Halothane and Forskolin on Platelet Cytosolic Ca (2+) Mobilization and Aggregation

Anesthesiology ◽

10.1097/00000542-199808000-00017 ◽

1998 ◽

Vol 89 (2) ◽

pp. 401-410 ◽

Cited By ~ 8

Author(s):

Francois Corbin ◽

Gilbert Blaise ◽

Remy Sauve

Keyword(s):

Platelet Aggregation ◽

Platelet Activating Factor ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Inhibitory Effect ◽

Signaling Cascade ◽

Aggregation Process ◽

Camp Production ◽

Biochemical Pathways ◽

Stimulation Of

Background Previous works have suggested that the impairment of platelet aggregation by halothane was partly related to a stimulation of cyclic adenosine monophosphate (cAMP) production, to an inhibitory effect on Ca2+ signaling, or both. Intracellular Ca2+ measurements therefore were undertaken, first to determine the critical steps in the platelet CaZ+ signaling cascade most likely to be affected by halothane or by an increase in cAMP production, and second to establish if the effect of halothane involves aggregation-related biochemical pathways triggered by an increase in internal Ca2+. Methods Human washed platelets were treated with halothane or forskolin for 5 min before application of either platelet-activating factor, thrombin, U46619, or thapsigargin. The cytosolic Ca2+ concentration ([Ca2+]i) was measured with the fluorescent Ca2+ indicator fura-2. Nephelometric measurements were also performed to assay the aggregation process. Results Our results indicate that pretreating platelets with halothane leads to a partial impairment of the [Ca2+]i increase induced either by U46619, thrombin, or platelet-activating factor, but this had no significant effect on the [Ca2+]i response triggered by thapsigargin. In addition, our results show that halothane inhibits platelet aggregation triggered by U46619, but not by thapsigargin. Conversely, forskolin completely inhibited the [Ca2+]i response to U46619 and thapsigargin and prevented platelet aggregation induced by both agonists. Conclusions These results suggest that halothane and cAMP exert their effects on platelet aggregation and Ca2+ signaling through different mechanisms, and that halothane cannot impair platelet aggregation independently of phospholipase C stimulation.

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Prevention of platelet aggregation and arterial thrombosis using a modified Shenzhu Guanxin Formula

Journal of International Medical Research ◽

10.1177/0300060520941326 ◽

2020 ◽

Vol 48 (10) ◽

pp. 030006052094132

Author(s):

Manting Huang ◽

Huanlin Wu ◽

Jianping Wu ◽

Qiuxiong Chen ◽

Dezhi Zou ◽

...

Keyword(s):

Platelet Aggregation ◽

Arterial Thrombosis ◽

Bleeding Time ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Dependent Manner ◽

Antithrombotic Agent ◽

Beneficial Effects ◽

Thrombosis Model ◽

Carotid Arterial

Objective Modified Shenzhu Guanxin Formula (mSGF) has beneficial effects in coronary artery disease. Previously, we found that mSGF inhibited platelet aggregation in rats. In the present study we further investigated the antiplatelet and antithrombotic activities of mSGF in rats. Methods Rats were orally administered mSGF (4.2, 8.4, or 16.8 g crude drug/kg), the adenosine 5′-diphosphate (ADP) receptor antagonist clopidogrel (7.875 mg/kg), or saline once a day for 7 days. The effects of mSGF on platelet aggregation were measured. Levels of cyclic adenosine monophosphate (cAMP) and phosphoinositide 3-kinase (PI3K) signaling were analyzed by ELISA and western blotting, respectively. The antithrombotic effect of mSGF was investigated using a FeCl3-induced carotid arterial thrombosis model and effects on bleeding time were assessed in a rat tail transection model. Results mSGF significantly inhibited ADP-induced platelet aggregation in a dose-dependent manner, elevated cAMP levels and inhibited phosphorylation of extracellular signal-regulated kinase (ERK) and PI3K/protein kinase B (Akt). Moreover, mSGF dose-dependently inhibited thrombosis in a FeCl3-induced carotid arterial thrombus model and had a significantly smaller effect on bleeding time compared with clopidogrel. Conclusions mSGF represents a potent and safe antithrombotic agent whose antiplatelet activity is probably mediated through blockade of PI3K/Akt signaling and increased cAMP generation.

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