Evaluation of potato tuber carboxypeptidase inhibitor with standard anti-thrombotic drugs in various thrombosis models

S. Bhatt, D.K. Pandey, K.S.R. Pai

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Abstract

Thrombosis is one of the major causes of death worldwide. It occurs due to imbalance between prothrombotic and fibrinolytic pathway. The clot formation activates the endogenous fibrinolytic system, for conversion of plasminogen to plasmin. Plasmin degrades the fibrin clot, restoring blood flow to vital organs. Thus, fibrinolysis is a physiological mechanism designed to remove intravascular thrombi while maintaining vascular patency. Several fibrinolytic drugs such as Streptokinase, recombinant t-PA and Reteplase are used clinically, principally to reperfuse the occluded coronary artery in diseases such as angina pectoris. However, these thrombolytics have many shortcomings such enhanced risk of bleeding such as GI haemorrhage. Present study was carried out for evaluation of potato tuber carboxypeptidase inhibitor, which is an inhibitor of thrombin activatable fibrinolysis inhibitor (TAFI) a newer target for fibrinolytic drugs which inhibits the conversion of plasminogen to plasmin with other standard drugs like aspirin and clopidogrel in models of thrombososis and coagulation.
Original languageEnglish
JournalInternational Journal of Pharma and Bio Sciences
Volume1
Issue number1
Publication statusPublished - 2010

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Carboxypeptidases
Fibrinolysin
Solanum tuberosum
Thrombosis
Fibrinolytic Agents
Plasminogen
clopidogrel
Vascular Patency
Carboxypeptidase B2
Pharmaceutical Preparations
Hemorrhage
Streptokinase
Angina Pectoris
Fibrinolysis
Coagulation
Fibrin
Aspirin
Coronary Artery Disease
Cause of Death
Blood

Cite this

@article{58ff8d4f1c66467087c8f1bf10d19e73,
title = "Evaluation of potato tuber carboxypeptidase inhibitor with standard anti-thrombotic drugs in various thrombosis models",
abstract = "Thrombosis is one of the major causes of death worldwide. It occurs due to imbalance between prothrombotic and fibrinolytic pathway. The clot formation activates the endogenous fibrinolytic system, for conversion of plasminogen to plasmin. Plasmin degrades the fibrin clot, restoring blood flow to vital organs. Thus, fibrinolysis is a physiological mechanism designed to remove intravascular thrombi while maintaining vascular patency. Several fibrinolytic drugs such as Streptokinase, recombinant t-PA and Reteplase are used clinically, principally to reperfuse the occluded coronary artery in diseases such as angina pectoris. However, these thrombolytics have many shortcomings such enhanced risk of bleeding such as GI haemorrhage. Present study was carried out for evaluation of potato tuber carboxypeptidase inhibitor, which is an inhibitor of thrombin activatable fibrinolysis inhibitor (TAFI) a newer target for fibrinolytic drugs which inhibits the conversion of plasminogen to plasmin with other standard drugs like aspirin and clopidogrel in models of thrombososis and coagulation.",
author = "S. Bhatt and D.K. Pandey and K.S.R. Pai",
note = "Cited By :1 Export Date: 10 November 2017 Correspondence Address: Bhatt, S.; Pharmacy Group, FD-III, Birla Institute of Technology and Science, Pilani, Rajasthan-333031, India; email: shvetankbhatt@gmail.com Chemicals/CAS: acetylsalicylic acid, 493-53-8, 50-78-2, 53663-74-4, 53664-49-6, 63781-77-1; clopidogrel, 113665-84-2, 120202-66-6, 90055-48-4, 94188-84-8; ferric oxide, 1309-37-1, 56449-54-8; plasmin, 9001-90-5, 9004-09-5; plasminogen, 9001-91-6 Manufacturers: Zydus, India References: Hendriks, D., Scharpe, S., Van sande, M., Characterization of a carboxypeptidase in human serum distinct from carboxypeptidase N (1989) J. Clin. Chem. Clin. Biochem, 27, pp. 277-285; Campbell, W., Okada, H., An arginine specific carboxypeptidase generated in blood during coagulation or inflammation which is unrelated to carboxypeptidase N or its subunits (1989) Biochem. Biophys. Res Commun, 162, pp. 933-939; Eaton, D.L., Malloy, B.E., Tsai, S.P., Isolation, molecular cloning, and partial characterization of a novel Carboxypeptidase B from human plasma (1991) J Biol Chem, 266 (32), pp. 21833-21838; Dundar, Y., Hill, R., Dickson, R., Comparative efficacy of thrombolytics in acute myocardial infarction: a systematic review (2003) Q J Med, 96, pp. 103-113; Gore, J.M., Granger, C.B., Simoons, M.L., Stroke after thrombolysis: mortality and functional outcomes in the GUSTO-I trial (1995) Circulation, 92, pp. 2811-2818; Meigs, J.B., D'agostino, R.B., Wilson, P.W.F., Risk variable clustering in the insulin resistance syndrome (1997) Diabetes, 46, pp. 1594-1600; Guven, G.S., Kilicaslan, A., Oz, S.G., (2006) Decrements in the Thrombin Activatable Fibrinolysis Inhibitor (TAFI) Levels in Association with Orlistat Treatment in Obesity Clinical and Applied Thrombosis/Hemostasis, 12 (3), pp. 364-368; Hass, J.M., Ryan, C.A., Methods Enzymol., 80, pp. 778-791; Ryan, C.A., Purification and properties of a carboxypeptidase inhibitor from potatoes (1974) J Biol Chem, 249, pp. 5495-5499; Anonymus, A., Randomized Blind Trial of Clopidogrel Versus Aspirin In Patients At Risk of Ischemic Events (CAPRIE). CAPRIE steering Committee (1996) Lancet, 348, pp. 1329-1339; Coukell, A., Markham, A., (1997) Clopidogrel. Drugs, 54, pp. 745-750; Gachet, C., Platelet activation by ADP: the role of ADP antagonists (2000) Ann. Med, 32 (SUPPL. 1), pp. 15-20. , 15-20; Hechler, B., Eckly, A., Ohlmann, P., Cazenave, J.P., Gahet, C., The p2y1 receptor, necessary but not sufficient to support full ADP induced platelet aggregation, is not the target of the drug Clopidogrel (1998) Br. J Haematol., 103, pp. 858-866; Bhawan, J., Joris, I., Girolami, U., Majno, J., Effect of cclusion on large vessels, I.A study of the rat carotid cartery (1977) Am. J Pathol., 88, pp. 355-380; Kurz, K.D., Main, B.W., Sandusky, G.E., Rat model of arterial thrombosis induced by ferric chloride (1990) Thromb. Res., 60, pp. 269-280; Wang, Y.X., Dong, N., Wu, C., Martin-McNulty, B., Fitch, R.M., Vicelette, J., Tran, K., Wu, Q., Lipopolysaccharide attenuates thrombolysis in batroxobin-induced lung vasculature fibrin deposition but not in ferrous chloride-induced carotid artery thrombus in rats: role of endogenous PAI-1 (2003) Thromb. Res., 111, pp. 381-387; Herbert, J.M., Bernat, A., Maffrand, J.P., Aprotinin reduces clopidogrel-induced prolongation of the bleeding time in the rat (1993) Thromb. Res., 71, pp. 433-441; Oldgren, J., Linder, R., Grip, L., Siegbahn, A., Wallentin, L., Activated partial thromboplastin time and clinical outcome after thrombin inhibition in unstable coronary artery disease (1999) Eur Heart J, 20 (22), pp. 1657-1666; Kurata, M., Noguchi, N., Kasuga, Y., Sugimoto, T., Tanaka, K., Hasegawa, T., Prolongation of PT and APTT under excessive anticoagulant in plasma from rats and dogs (1998) J Toxicol Sci., 23 (2), pp. 149-153; Nagashima, M., Yin, Z.F., Zhao, L., White, K., Zhu, Y., Lasky, N., Halks-Miller, M., Morser, J., Thrombin-activatable fibrinolysis inhibitor (TAFI) deficiency is compatible with murine life (2002) J Clin Invest, 109, pp. 101-110",
year = "2010",
language = "English",
volume = "1",
journal = "International Journal of Pharma and Bio Sciences",
issn = "0975-6299",
publisher = "International Journal of Pharma and Bio Sciences",
number = "1",

}

TY - JOUR

T1 - Evaluation of potato tuber carboxypeptidase inhibitor with standard anti-thrombotic drugs in various thrombosis models

AU - Bhatt, S.

AU - Pandey, D.K.

AU - Pai, K.S.R.

N1 - Cited By :1 Export Date: 10 November 2017 Correspondence Address: Bhatt, S.; Pharmacy Group, FD-III, Birla Institute of Technology and Science, Pilani, Rajasthan-333031, India; email: shvetankbhatt@gmail.com Chemicals/CAS: acetylsalicylic acid, 493-53-8, 50-78-2, 53663-74-4, 53664-49-6, 63781-77-1; clopidogrel, 113665-84-2, 120202-66-6, 90055-48-4, 94188-84-8; ferric oxide, 1309-37-1, 56449-54-8; plasmin, 9001-90-5, 9004-09-5; plasminogen, 9001-91-6 Manufacturers: Zydus, India References: Hendriks, D., Scharpe, S., Van sande, M., Characterization of a carboxypeptidase in human serum distinct from carboxypeptidase N (1989) J. Clin. Chem. Clin. Biochem, 27, pp. 277-285; Campbell, W., Okada, H., An arginine specific carboxypeptidase generated in blood during coagulation or inflammation which is unrelated to carboxypeptidase N or its subunits (1989) Biochem. Biophys. Res Commun, 162, pp. 933-939; Eaton, D.L., Malloy, B.E., Tsai, S.P., Isolation, molecular cloning, and partial characterization of a novel Carboxypeptidase B from human plasma (1991) J Biol Chem, 266 (32), pp. 21833-21838; Dundar, Y., Hill, R., Dickson, R., Comparative efficacy of thrombolytics in acute myocardial infarction: a systematic review (2003) Q J Med, 96, pp. 103-113; Gore, J.M., Granger, C.B., Simoons, M.L., Stroke after thrombolysis: mortality and functional outcomes in the GUSTO-I trial (1995) Circulation, 92, pp. 2811-2818; Meigs, J.B., D'agostino, R.B., Wilson, P.W.F., Risk variable clustering in the insulin resistance syndrome (1997) Diabetes, 46, pp. 1594-1600; Guven, G.S., Kilicaslan, A., Oz, S.G., (2006) Decrements in the Thrombin Activatable Fibrinolysis Inhibitor (TAFI) Levels in Association with Orlistat Treatment in Obesity Clinical and Applied Thrombosis/Hemostasis, 12 (3), pp. 364-368; Hass, J.M., Ryan, C.A., Methods Enzymol., 80, pp. 778-791; Ryan, C.A., Purification and properties of a carboxypeptidase inhibitor from potatoes (1974) J Biol Chem, 249, pp. 5495-5499; Anonymus, A., Randomized Blind Trial of Clopidogrel Versus Aspirin In Patients At Risk of Ischemic Events (CAPRIE). CAPRIE steering Committee (1996) Lancet, 348, pp. 1329-1339; Coukell, A., Markham, A., (1997) Clopidogrel. Drugs, 54, pp. 745-750; Gachet, C., Platelet activation by ADP: the role of ADP antagonists (2000) Ann. Med, 32 (SUPPL. 1), pp. 15-20. , 15-20; Hechler, B., Eckly, A., Ohlmann, P., Cazenave, J.P., Gahet, C., The p2y1 receptor, necessary but not sufficient to support full ADP induced platelet aggregation, is not the target of the drug Clopidogrel (1998) Br. J Haematol., 103, pp. 858-866; Bhawan, J., Joris, I., Girolami, U., Majno, J., Effect of cclusion on large vessels, I.A study of the rat carotid cartery (1977) Am. J Pathol., 88, pp. 355-380; Kurz, K.D., Main, B.W., Sandusky, G.E., Rat model of arterial thrombosis induced by ferric chloride (1990) Thromb. Res., 60, pp. 269-280; Wang, Y.X., Dong, N., Wu, C., Martin-McNulty, B., Fitch, R.M., Vicelette, J., Tran, K., Wu, Q., Lipopolysaccharide attenuates thrombolysis in batroxobin-induced lung vasculature fibrin deposition but not in ferrous chloride-induced carotid artery thrombus in rats: role of endogenous PAI-1 (2003) Thromb. Res., 111, pp. 381-387; Herbert, J.M., Bernat, A., Maffrand, J.P., Aprotinin reduces clopidogrel-induced prolongation of the bleeding time in the rat (1993) Thromb. Res., 71, pp. 433-441; Oldgren, J., Linder, R., Grip, L., Siegbahn, A., Wallentin, L., Activated partial thromboplastin time and clinical outcome after thrombin inhibition in unstable coronary artery disease (1999) Eur Heart J, 20 (22), pp. 1657-1666; Kurata, M., Noguchi, N., Kasuga, Y., Sugimoto, T., Tanaka, K., Hasegawa, T., Prolongation of PT and APTT under excessive anticoagulant in plasma from rats and dogs (1998) J Toxicol Sci., 23 (2), pp. 149-153; Nagashima, M., Yin, Z.F., Zhao, L., White, K., Zhu, Y., Lasky, N., Halks-Miller, M., Morser, J., Thrombin-activatable fibrinolysis inhibitor (TAFI) deficiency is compatible with murine life (2002) J Clin Invest, 109, pp. 101-110

PY - 2010

Y1 - 2010

N2 - Thrombosis is one of the major causes of death worldwide. It occurs due to imbalance between prothrombotic and fibrinolytic pathway. The clot formation activates the endogenous fibrinolytic system, for conversion of plasminogen to plasmin. Plasmin degrades the fibrin clot, restoring blood flow to vital organs. Thus, fibrinolysis is a physiological mechanism designed to remove intravascular thrombi while maintaining vascular patency. Several fibrinolytic drugs such as Streptokinase, recombinant t-PA and Reteplase are used clinically, principally to reperfuse the occluded coronary artery in diseases such as angina pectoris. However, these thrombolytics have many shortcomings such enhanced risk of bleeding such as GI haemorrhage. Present study was carried out for evaluation of potato tuber carboxypeptidase inhibitor, which is an inhibitor of thrombin activatable fibrinolysis inhibitor (TAFI) a newer target for fibrinolytic drugs which inhibits the conversion of plasminogen to plasmin with other standard drugs like aspirin and clopidogrel in models of thrombososis and coagulation.

AB - Thrombosis is one of the major causes of death worldwide. It occurs due to imbalance between prothrombotic and fibrinolytic pathway. The clot formation activates the endogenous fibrinolytic system, for conversion of plasminogen to plasmin. Plasmin degrades the fibrin clot, restoring blood flow to vital organs. Thus, fibrinolysis is a physiological mechanism designed to remove intravascular thrombi while maintaining vascular patency. Several fibrinolytic drugs such as Streptokinase, recombinant t-PA and Reteplase are used clinically, principally to reperfuse the occluded coronary artery in diseases such as angina pectoris. However, these thrombolytics have many shortcomings such enhanced risk of bleeding such as GI haemorrhage. Present study was carried out for evaluation of potato tuber carboxypeptidase inhibitor, which is an inhibitor of thrombin activatable fibrinolysis inhibitor (TAFI) a newer target for fibrinolytic drugs which inhibits the conversion of plasminogen to plasmin with other standard drugs like aspirin and clopidogrel in models of thrombososis and coagulation.

M3 - Article

VL - 1

JO - International Journal of Pharma and Bio Sciences

JF - International Journal of Pharma and Bio Sciences

SN - 0975-6299

IS - 1

ER -