ozagrel has been researched along with Thrombosis* in 9 studies
1 review(s) available for ozagrel and Thrombosis
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Progress of thrombus formation and research on the structure-activity relationship for antithrombotic drugs.
Many populations suffer from thrombotic disorders such as stroke, myocardial infarction, unstable angina and thromboembolic disease. Thrombus is one of the major threatening factors to human health and the prevalence of cardio-cerebrovascular diseases induced by thrombus is growing worldwide, even some persons got rare and severe blood clots after receiving the AstraZeneca COVID vaccine unexpectedly. In terms of mechanism of thrombosis, antithrombotic drugs have been divided into three categories including anticoagulants, platelet inhibitors and fibrinolytics. Nowadays, a large number of new compounds possessing antithrombotic activities are emerging in an effort to remove the inevitable drawbacks of previously approved drugs such as the high risk of bleeding, a slow onset of action and a narrow therapeutic window. In this review, we describe the causes and mechanisms of thrombus formation firstly, and then summarize these reported active compounds as potential antithrombotic candidates based on their respective mechanism, hoping to promote the development of more effective bioactive molecules for treating thrombotic disorders. Topics: Fibrinolytic Agents; Humans; Molecular Structure; Thrombosis | 2022 |
8 other study(ies) available for ozagrel and Thrombosis
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[The study of relationship between platelet function and thrombus in patients with essential thrombocythaemia].
To observe the influence of the plasma thromboxane B2 (TXB2), 6-keto-PGF1alpha, CD62P and PAC-1 and Thrombus in patients with primary thrombocytosis (ET). To observe the effect of sodium ozagrel to prevent and treat thrombosis in patients with ET.. The subjects including 48 patients with ET. All patients were measured the plasma TXB2, 6-keto-PGF1alpha, CD62P and PAC-1 before and after treatment with or without sodium ozagrel.. The plasma levels of CD62P, PAC-1, TXB2, 6-keto-PGF1alpha and TXA2/PGI2 in the patients with ET were significantly higher than the normal people (P < 0.01). The levels of CD62P, PAC-1, TXB2, TXB2/6-keto-PGF1alpha in patients with treatment of sodium ozagrel were higher than patients without treatment of sodium ozagrel (P < 0.01). The plasma levels of CD62P, PAC-1 and TXA2/PGI2 in patients with treatment of sodium ozagrel and that in normal people had no significant distinction (P < 0.01). All the index of conventional therapy group were higher than normal people (P < 0.01) but had no significant distinction with the patients before conventional treating. The incidence of thrombus in patients treated with sodium ozagrel was lower than patients treated without sodium ozagrel (P < 0.05).. With the treatment of sodium ozagrel in patients with ET, the CD62P, PAC-1, TXB2 and TXA2/PGI2 of plasma could be decreased. And the incidence of thrombus was decreased. Topics: 6-Ketoprostaglandin F1 alpha; Adult; Antibodies, Monoclonal; Blood Platelets; Female; Humans; Male; Methacrylates; Middle Aged; P-Selectin; Receptors, Fibrinogen; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; Thrombocythemia, Essential; Thrombosis; Thromboxane A2; Thromboxane B2 | 2010 |
[Effects of sodium ozagrel in primary thrombocytosis combined with thrombosis].
This study was aimed to investigate the incidence of thrombosis in patients with primary thrombocytosis (PT) and its correlation with function changes of platelets, and to explore the effect of thromboxane A2 (TXA2) inhibitor-ozagrel sodium on platelet activity and its efficacy for prevention and treatment of thrombosis. The CD62P and PAC-1 levels on platelet surface were detected by flow cytometry; the levels of TXB2 (metabolic product of TXA2) and 6-keto-PGFIalpha (metabolic product of prostacyclin) were detected by FLISA. The function change of platelets and its correlation with thrombosis were observed and compared in PT patients with and without thrombosis. The results indicated that the TXB2, PAC-1 and CD62P level, and TXB2/6-keto-PGF1alpha ratio in PT patients with thrombosis were higher than those in PT patients without thrombosis before treatment with ozagrel sodium (p<0.01). After treatment with ozagrel sodium, the function indexes of platelets such as CD62P, PAC-1, TXB2 and TXB2/6-keto-PGF1alpha except 6-keto-PGF1alpha in PT patients with and without thrombosis decreased obviously (p<0.01), but there was no significant difference in TXB2, 6-keto-PGF1alpha and TXB2/6-keto-PGF1alpha levels between PT patients with and without thrombosis except CD62P and PAC-1. It is concluded that the multi-index of platelets in PT patients with thrombosis are higher than that in PT patients without thrombosis, the activation of platelet function is a high risk factor for thrombosis of PT patients. The ozagrel sodium can obviously reduce the platelet activation, decrease the production of TXA2 and ameliorate the TXB2/6-keto-PGF1alpha ratio. The ozagrel sodium not only possesses therapeutic effect, but also preventive efficacy for thrombosis. Topics: Adolescent; Adult; Aged; Female; Fibrinolytic Agents; Humans; Male; Methacrylates; Middle Aged; Thrombocythemia, Essential; Thrombosis; Young Adult | 2009 |
Role for thromboxane A2 from glomerular thrombi in nephropathy with type 2 diabetic rats.
We used rats (the Otsuka Long-Evans Tokushima Fatty strain) as a model of type 2 diabetes to find whether thromboxane (TX) A2 is involved in diabetic nephropathy, and if so, to identify where it is synthesized. We measured urinary excretion of TXB2 and 2,3-dinor-TXB2 in rats up to 60 weeks of age as markers of renal and platelet synthesis of TXA2, respectively. Some diabetic rats were given daily oral doses of OKY-046 (100 mg/kg), a TXA2 synthase inhibitor, starting when they were 10 weeks of age. Healthy Long-Evans Tokushima Otsuka rats served as the controls. Urinary excretion of protein was greater in diabetic rats at 26 weeks than in controls, and the difference increased with age. Urinary excretion of TXB2 by diabetic rats was about 150% that of controls at 14 weeks, and remained at that level. In diabetic rats, urinary excretion of 2,3-dinor-TXB2 increased with age in parallel to increases in proteinuria, but in controls, excretion of these metabolites did not change with age. In diabetic rats, OKY-046 prevented the increase in urinary excretion of both metabolites, and decreased the proteinuria. Histologic examination at 60 weeks showed intraglomerular thrombi in diabetic rats but not in controls. OKY-046 reduced intraglomerular thrombi formation and the score for glomerulosclerosis. When platelet aggregation began, more TXA2 than before was released from the thrombi that formed, and the TXA2 contributed to the progress of nephropathy in this rat model of type 2 diabetes. Topics: 6-Ketoprostaglandin F1 alpha; Aging; Animals; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Disease Progression; Enzyme Inhibitors; Glomerular Mesangium; Male; Methacrylates; Prostaglandins; Proteinuria; Rats; Rats, Inbred OLETF; Thrombosis; Thromboxane A2; Thromboxane-A Synthase | 2003 |
Effect of ozagrel, a selective thromboxane A2-synthetase inhibitor, on cerebral infarction in rats. Comparative study with norphenazone, a free-radical scavenger.
The effects of ozagrel (CAS 82571-53-7), a thromboxane A2-synthetase inhibitor, and norphenazone (CAS 89-25-8), a free-radical scavenger, on cerebral infarction were assessed using the suture-induced middle cerebral artery occlusion (MCAO) model and a microthrombosis model. In the former model, the middle cerebral artery was occluded for 2 h, and the infarction area and volume were evaluated 24 h after the start of reperfusion. In the latter model, microthrombosis were induced by two injections of sodium laurate (interval, 2 days) into the internal carotid artery, and the neurologic deficits were evaluated on the day afer the 2nd injection. Ozagrel at 3 mg/kg decreased both the area and volume of the cortical infarction after ischemia-reperfusion of the middle cerebral artery. Ozagrel also had suppressive effects on the neurologic deficits in the microthrombosis model. Norphenazone at 1 and 3 mg/kg had no clear effects in either model. Since the suture-induced MCAO model and the microthrombosis model are models for occlusion-reperfusion of the major cerebral arteries and lacunar infarction, respectively, these results suggest a highly beneficial effect of ozagrel in the clinical therapy for stroke. Topics: Animals; Antipyrine; Edaravone; Enzyme Inhibitors; Free Radical Scavengers; Infarction, Middle Cerebral Artery; Male; Methacrylates; Middle Cerebral Artery; Optic Chiasm; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thrombosis; Thromboxane-A Synthase | 2003 |
Antiplatelet and antithrombotic effects of YM337, the Fab fragment of a humanized anti-GPIIb/IIIa monoclonal antibody in monkeys.
The antiplatelet and antithrombotic effects of the Fab fragment of the humanized antiplatelet glycoprotein (GP) IIb/IIIa monoclonal antibody C4G1 (YM337) were investigated in monkeys. First, the relationship between the inhibition of platelet aggregation and the prolongation of bleeding time was studied in rhesus monkeys. YM337 dose-dependently inhibited ex vivo platelet aggregation, with complete inhibition at doses higher than 0.25 mg/kg intravenous injection or 1.5 micrograms/kg/min infusion. At 0.25 mg/kg bolus injection followed by 1.5 micrograms/kg/min infusion, YM337 immediately and continuously inhibited platelet aggregation during the 6-h infusion period with platelet aggregation rapidly returning to over 50% of baseline within 1 h after the cessation of infusion. Template-bleeding time was significantly prolonged during the period of complete inhibition of platelet aggregation. Second, the antithrombotic effects of YM337 were investigated in a photochemically-induced thrombosis model in squirrel monkeys. YM337 at a dose of 1 mg/kg intravenous injection followed by 6 micrograms/kg/min infusion for 60 min prevented occlusive thrombus formation in all 4 monkeys. In contrast, time to occlusive thrombus formation did not change on intravenous bolus injection of aspirin 17 mg/kg (11.3 +/- 5.2 min) or sodium ozagrel (9.4 +/- 3.0 min) compared with saline (13.3 +/- 4.0 min). YM337 but not aspirin or sodium ozagrel significantly inhibited ex vivo ADP-induced platelet aggregation, while all drugs completely inhibited arachidonic acid-induced platelet aggregation. However, while aspirin and sodium ozagrel inhibited the thromboxane B2 generation accompanying arachidonic acid-induced platelet aggregation, YM337 had no effect on this variable. Platelet counts and bleeding time showed no significant change in any group in this squirrel monkey model. These results indicate that YM337, with a short half-life, may be a useful therapeutic agent in patients with thrombotic disorders. Topics: Animals; Antibodies, Monoclonal; Aspirin; Bleeding Time; Dose-Response Relationship, Immunologic; Fibrinolytic Agents; Immunoglobulin Fab Fragments; Macaca mulatta; Methacrylates; Photochemistry; Platelet Aggregation Inhibitors; Platelet Count; Platelet Glycoprotein GPIIb-IIIa Complex; Random Allocation; Saimiri; Thrombosis | 1996 |
Effects of thromboxane A2 synthase inhibitors (CV-4151 and ozagrel), aspirin, and ticlopidine on the thrombosis caused by endothelial cell injury.
The antiplatelet and antithrombotic effects of CV-4151 (isbogrel), a potent selective thromboxane A2 (TXA2) synthase inhibitor, were compared with those of ozagrel (OKY-046), aspirin, and ticlopidine in rats. Two hours after oral administration, CV-4151, ozagrel and aspirin inhibited blood TXA2 generation with ID50 values of 0.04, 0.3 and 6.4 mg/kg, respectively. These values were similar to the oral ID50 values of CV-4151 (0.06 mg/kg), ozagrel (0.92 mg/kg) and aspirin (7.0 mg/kg) for arachidonic acid (AA)-induced platelet aggregation ex vivo. Two hours after p.o. administration, CV-4151 and ozagrel inhibited femoral vein platelet-rich thrombosis caused by endothelial injury with ID50 values of 2.46 and 13.7 mg/kg, respectively. However, aspirin (100 mg/kg, p.o.) only slightly inhibited the thrombosis. Ticlopidine (300 mg/kg, p.o.) slightly but significantly inhibited AA-induced and ADP-induced platelet aggregation, however, it potently inhibited the thrombosis. CV-4151 and ozagrel given by i.v. injection showed therapeutic effects on the thrombosis with ED50 values of 0.026 and 0.066 mg/kg, respectively. These values were similar to the i.v. ED50 values of CV-4151 (0.0056 mg/kg) and ozagrel (0.042 mg/kg) for blood TXA2 generation. However, aspirin (30 mg/kg, i.v.) only moderately reduced the thrombosis. CV-4151 (> 0.3 mg/kg, p.o.), ozagrel (> 3 mg/kg, p.o.) and ticlopidine (300 mg/kg, p.o.) all significantly prolonged tail bleeding time. Aspirin (100 mg/kg, p.o.) tended to prolong the bleeding time. The antiplatelet and antithrombotic effects of CV-4151 are more potent than those of ozagrel, aspirin and ticlopidine in rats. CV-4151 may therefore be a useful drug for the treatment of thrombotic diseases. Topics: Animals; Aspirin; Bleeding Time; Endothelium, Vascular; Fatty Acids, Monounsaturated; Femoral Vein; Male; Methacrylates; Platelet Aggregation; Pyridines; Rats; Rats, Sprague-Dawley; Thrombosis; Thromboxane-A Synthase; Thromboxanes; Ticlopidine | 1995 |
The combination of thrombin inhibitor and thromboxane synthase inhibitor on experimental thrombosis and bleeding.
Topics: Animals; Antithrombins; Arginine; Bleeding Time; Drug Synergism; Drug Therapy, Combination; Infusions, Intravenous; Male; Methacrylates; Pipecolic Acids; Rabbits; Sulfonamides; Thrombin; Thrombosis; Thromboxane-A Synthase | 1995 |
Protective effects of thromboxane A2 synthetase inhibitors on endotoxin shock.
To elucidate the role of thromboxane A2 in the development of endotoxin shock following administration of endotoxin, the effects of three thromboxane A2 synthetase inhibitors, (E)-3-(4-(1-imidazolyl)phenyl)-2-propenoic acid hydrochloride monohydrate (OKY-046), sodium (E)-3-(4-(3-pyridylmethyl)phenyl)-2-methylacrylate (OKY-1581) and imidazole were examined. Intravenous administration of E. Coli endotoxin (3 mg/kg) produced shock and all rats died within ten hours. Pretreatment with thromboxane A2 synthetase inhibitors markedly improved the survival rates. The untreated endotoxin shock group showed marked increase in thromboxane B2 levels in the venous blood, while no such changes were seen in the pretreated groups. There were no statistically significant differences in 6-keto prostaglandin F1 alpha levels in the venous blood. In the untreated shock group, microthrombi were observed in 64% of the glomeruli in the kidneys two hours after endotoxin injection. In the groups pretreated with OKY-046, OKY-1581 and imidazole, microthrombi were seen only in 22, 19 and 24%, respectively. Thus, thromboxane A2 plays an important role in the development of endotoxin shock and thromboxane A2 synthetase inhibitors, in particular OKY-046 and -1581, are prophylactic. Topics: Animals; Fibrinogen; Glucuronidase; Kidney; Male; Methacrylates; Oxidoreductases; Platelet Count; Rats; Rats, Inbred Strains; Shock, Septic; Thrombosis; Thromboxane A2; Thromboxane B2; Thromboxane-A Synthase; Thromboxanes | 1983 |