New Flavonol Oligoglycosides and Polyacylated Sucroses with Inhibitory Effects on Aldose Reductase and Platelet Aggregation from the Flowers ofPrunus mume1

2002 ◽  
Vol 65 (8) ◽  
pp. 1151-1155 ◽  
Author(s):  
Masayuki Yoshikawa ◽  
Toshiyuki Murakami ◽  
Tomoko Ishiwada ◽  
Toshio Morikawa ◽  
Masatomo Kagawa ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Aldose Reductase ◽  
Inhibitory Effects

scholarly journals Inhibitory Effects of 2'-Hydroxychalcones on Rat Lens Aldose Reductase and Rat Platelet Aggregation.

2000 ◽  
Vol 48 (11) ◽  
pp. 1786-1789 ◽  
Author(s):  
Soon Sung LIM ◽  
Sang Hoon JUNG ◽  
Jun JI ◽  
Kuk Hyun SHIN ◽  
Sam Rok KEUM
Keyword(s):  
Platelet Aggregation ◽  
Aldose Reductase ◽  
Inhibitory Effects ◽  
Rat Lens Aldose Reductase

The Effects of Brinolase (Fibrinolytic Enzyme from Aspergillus Oryzae) on Platelet Aggregation of Dog and Man

1972 ◽  
Vol 28 (01) ◽  
pp. 031-048 ◽  
Author(s):  
W. H. E Roschlau ◽  
R Gage
Keyword(s):  
Platelet Aggregation ◽  
Aspergillus Oryzae ◽  
Degradation Products ◽  
Blood Platelet ◽  
Human Platelets ◽  
Fibrinolytic Enzyme ◽  
Inhibitory Effects ◽  
Blood Platelet Aggregation

SummaryInhibition of blood platelet aggregation by brinolase (fibrinolytic enzyme from Aspergillus oryzae) has been demonstrated with human platelets in vitro and with dog platelets in vivo and in vitro, using both ADP and collagen as aggregating stimuli. It is suggested that the optimal inhibitory effects of brinolase occur indirectly through the generation of plasma fibrinogen degradation products, without compromising platelet viability, rather than by direct proteolysis of platelet structures.

scholarly journals Amide Derivatives of Ginkgolide B and Their Inhibitory Effects on PAF-Induced Platelet Aggregation

ACS Omega ◽  
2021 ◽  
Author(s):  
Qiang Shang ◽  
Xiaobo Zhou ◽  
Ming-Rong Yang ◽  
Jing-Guang Lu ◽  
Yu Pan ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Ginkgolide B ◽  
Inhibitory Effects ◽  
Amide Derivatives ◽  
Derivatives Of

Inhibitory effect of pyridyloxy- or phenoxylphenoxyalkanate derivatives on rat lens aldose reductase and rat platelet aggregation

2004 ◽  
Vol 56 (7) ◽  
pp. 941-945 ◽  
Author(s):  
Soon Sung Lim ◽  
Kuk Hyun Shin ◽  
Sang Hoon Jung ◽  
Kye Jung Shin ◽  
Dong Chan Kim ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Aldose Reductase ◽  
Inhibitory Effect ◽  
Rat Lens Aldose Reductase

Inhibitory effects of Qushuanling Capsule (祛栓灵胶囊) on thrombus formation and platelet aggregation in rats

2012 ◽  
Vol 19 (2) ◽  
pp. 137-142
Author(s):  
Jie Xue ◽  
Ke-ping Zhang ◽  
Lu-jia Zhu ◽  
Mei-lin Xie ◽  
Hong-quan Zhang
Keyword(s):  
Platelet Aggregation ◽  
Thrombus Formation ◽  
Inhibitory Effects

Combined blockade of thrombin anion binding exosite-1 and PAR4 produces synergistic antiplatelet effect in human platelets

2011 ◽  
Vol 105 (01) ◽  
pp. 88-95 ◽  
Author(s):  
Wei-Ya Wang ◽  
Chien-Kei Wei ◽  
Che-Ming Teng ◽  
Chin-Chung Wu
Keyword(s):  
Platelet Aggregation ◽  
Active Site ◽  
Antithrombotic Therapy ◽  
Specific Binding ◽  
Anticoagulant Activity ◽  
Human Platelets ◽  
Anion Binding ◽  
Inhibitory Effects ◽  
Clotting Time ◽  
Potential Strategy

SummaryThrombin exosite-1 mediates the specific binding of thrombin with fibrinogen and protease-activated receptor (PAR) 1. Exosite-1 inhibitors have been shown to effectively decrease the clotting activity of thrombin, while their antiplatelet effects are relatively weak. In the present study, the inhibitory effects of two exosite-1 inhibitors, hirugen and HD1, but not the exosite-2 inhibitor HD22, on thrombin-induced platelet aggregation and P-selectin expression were dramatically enhanced by a PAR4 antagonist, YD-3. In contrast, the PAR1 antagonist SCH-79797 did not affect the antiplatelet effects of exosite-1 inhibitors. The exosite-1 inhibitors and YD-3 prevented the Ca2+ spike and the prolonged Ca2+ response in thrombin-stimulated platelets, respectively; and combination of these two classes of agents led to abolishment of Ca2+ signal. Unlike exosite-1 inhibitors, the antiplatelet effects of the active site inhibitor PPACK and the bivalent inhibitor bivalirudin were not significantly enhanced by YD-3. In addition, the platelet-stimulating activity of γ-thrombin, an autolytic product of α-thrombin which lacks exosite-1, was inhibited by YD-3. These results suggest that the synergistic antiplatelet effects of exosite-1 inhibitor and PAR4 antagonist are resulted from combined blockade of PAR1 and PAR4 in platelets. In fibrinogen or plasma clotting assay, YD-3 neither prolonged the clotting time on its own nor enhanced the anticoagulant activity of exosite-1 inhibitors. Therefore, the combined blockade of exosite-1 and PAR4 may offer a potential strategy for improving the balance of benefits and risks of antithrombotic therapy.

Roles of Cyclic Nucleotides in the Inhibition of Platelet Function by Physiolocic and Pharmacological Agents

1979 ◽  
Author(s):  
R.J. Haslam
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Platelet Function ◽  
Inhibitory Effects ◽  
Pharmacological Agents ◽  
Arterial Blood ◽  
Cyclic Cmp ◽  
Amp Inhibition

Cyclic AMP mediates the inhibitions of platelet aggregation caused by PCI2, PGE1 and PGD2. Thus, these compounds activate platelet adenylate cyclase and Increase platelet cyclic AMP; their inhibitory effects are blockod by inhibitor? of adenylate cyclase, are potentiated by inhibitors of cyclic AKP phosphodiesterase and are mimicked hy N6 ,2'-0-dibutyryl cyclic AMP. Inhibition of adenylate cyclase does not potentiate platelet aggregation in the absence of inhibitory prostaglandins, indicating that platelet cyclic AMP is too low to affect aggregation under these conditions. To determine whether platelets in the circulation are exposed to agents that increase platelet cyclic AMP, washed rabbi platelets labelled with [3H] adenine were incubated with rabbit arterial blood under various conditions; any increases in cyclic [3H]AMP were measured. These experiments showed that freshly taken rabbit arterial blood does not normally contain any factors that can increase platelet cyclic AMP sufficiently to affect platelet function; specifically, circulating PGI2 was less than 0.1 pmol/ml of blood. It follows that increases in cyclic AMP in circulating rabbit platelets must occur only locally or under special conditions. The role of the moderate increases in platelet cyclic CMP caused by aggregating agents remains uncertain, but the inhibition of aggregation by compounds such as sodium nitroprusside that increase cyclic CMP up to 100-fold suggests that cyclic CMP may, like cyclic AMP, be an inhibitory mediator.

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