A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation
Objective: Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced platelet aggregation. Met...
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| Veröffentlicht in: | Pharmazie 2014-08, Vol.69 (8), p.615-620 |
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| creator | Zhou, Kai Li, Xiaoli Du, Qin Li, Defeng Hu, Mo Yang, Xiaojia Jiang, Qi Li, Zhubo |
| description | Objective: Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced
platelet aggregation. Methods: Caffeic acid phenethyl ester (CAPE) is an active component in propolis. CAPE-NO2 is a nitro derivative of CAPE. Its effects on rat platelet aggregation induced by collagen were tested in vitro and the potential mechanisms underlying the
activities were investigated. Results: CAPE-NO2 significantly inhibited collagen-induced platelet aggregation in a concentration-dependent manner. It also reduced TXB2 formation and COX-1 activity in collagen-activated platelets. Moreover, CAPE-NO2 caused
an increase in NO production and cGMP levels and attenuated 5-HT release in the collagen-activated platelets. Conclusion: These findings suggest that the inhibitory mechanism of CAPE-NO2 on collagen-induced platelet aggregation might be associated with the down-regulation
of TXB2, COX-1 and 5-HT and the elevation of NO and cGMP production. These indicators are closely related to platelet function. So CAPE-NO2 may be a promising candidate for the extension of the current spectrum of antiplatelet drugs. |
| doi_str_mv | 10.1691/ph.2014.3970 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1558523846</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><ingid>govi/pharmaz/2014/00000069/00000008/art00009</ingid><sourcerecordid>1558523846</sourcerecordid><originalsourceid>FETCH-LOGICAL-i343t-124b39050d0578f2c62257bcb35b865de6ecd194ddaf041e849b9b1fa8c3c8643</originalsourceid><addsrcrecordid>eNp1kb1vFDEQxV2ASEjoqJFLmr34e-3ydASIFEEKUlte27vnyOdd1t6Tkr8eb-6QaHAzT57nnzxvAPiI0QYLhW-m_YYgzDZUtegNuESI4qbFjF2A9zk_IUQEEfIduCAcc8lbegn6LdxtH26hSSaOw-KhyTCNRx_rTQlTNMVHX6AZfCrQ932woar4DEPahy6UDO0Y49puQnKL9Q7-82iY_WBKGNM1eNubmP2Hc70Cj19vf-2-N_c_v93ttvdNoIyWBhPWUYU4coi3sidWEMLbznaUd1Jw54W3DivmnOkRw14y1akO90ZaaqVg9Ap8PnGnefy9-Fz0IWTr6w-TH5esMa9zEyqZqNZPZ-vSHbzT0xwOZn7Wf7Ophi8nQ0jr9EY_jctcY8p6GI9BT3szH8yLXgPX6PUIdRZIajOXVaiK-fEfTLAn0rqmdUv6KFSSFUgwkphqjJHSzvdmiUUXM-vhRWdF_wBthZS2</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1558523846</pqid></control><display><type>article</type><title>A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation</title><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Zhou, Kai ; Li, Xiaoli ; Du, Qin ; Li, Defeng ; Hu, Mo ; Yang, Xiaojia ; Jiang, Qi ; Li, Zhubo</creator><creatorcontrib>Zhou, Kai ; Li, Xiaoli ; Du, Qin ; Li, Defeng ; Hu, Mo ; Yang, Xiaojia ; Jiang, Qi ; Li, Zhubo</creatorcontrib><description>Objective: Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced
platelet aggregation. Methods: Caffeic acid phenethyl ester (CAPE) is an active component in propolis. CAPE-NO2 is a nitro derivative of CAPE. Its effects on rat platelet aggregation induced by collagen were tested in vitro and the potential mechanisms underlying the
activities were investigated. Results: CAPE-NO2 significantly inhibited collagen-induced platelet aggregation in a concentration-dependent manner. It also reduced TXB2 formation and COX-1 activity in collagen-activated platelets. Moreover, CAPE-NO2 caused
an increase in NO production and cGMP levels and attenuated 5-HT release in the collagen-activated platelets. Conclusion: These findings suggest that the inhibitory mechanism of CAPE-NO2 on collagen-induced platelet aggregation might be associated with the down-regulation
of TXB2, COX-1 and 5-HT and the elevation of NO and cGMP production. These indicators are closely related to platelet function. So CAPE-NO2 may be a promising candidate for the extension of the current spectrum of antiplatelet drugs.</description><identifier>ISSN: 0031-7144</identifier><identifier>DOI: 10.1691/ph.2014.3970</identifier><identifier>PMID: 25158573</identifier><language>eng</language><publisher>Germany: Govi-Verlag</publisher><subject>Animals ; Blood Platelets - drug effects ; Blood Platelets - metabolism ; Caffeic Acids - chemical synthesis ; Caffeic Acids - chemistry ; Caffeic Acids - pharmacology ; Collagen - antagonists & inhibitors ; Collagen - pharmacology ; Cyclic AMP - biosynthesis ; Cyclooxygenase 1 - biosynthesis ; In Vitro Techniques ; Indicators and Reagents ; Male ; Nitric Oxide - blood ; Phenylethyl Alcohol - analogs & derivatives ; Phenylethyl Alcohol - chemical synthesis ; Phenylethyl Alcohol - chemistry ; Phenylethyl Alcohol - pharmacology ; Platelet Aggregation - drug effects ; Platelet Aggregation Inhibitors - chemical synthesis ; Platelet Aggregation Inhibitors - pharmacology ; Rats ; Rats, Sprague-Dawley ; Serotonin - blood ; Thromboxane B2 - biosynthesis</subject><ispartof>Pharmazie, 2014-08, Vol.69 (8), p.615-620</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>288,314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25158573$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Kai</creatorcontrib><creatorcontrib>Li, Xiaoli</creatorcontrib><creatorcontrib>Du, Qin</creatorcontrib><creatorcontrib>Li, Defeng</creatorcontrib><creatorcontrib>Hu, Mo</creatorcontrib><creatorcontrib>Yang, Xiaojia</creatorcontrib><creatorcontrib>Jiang, Qi</creatorcontrib><creatorcontrib>Li, Zhubo</creatorcontrib><title>A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation</title><title>Pharmazie</title><addtitle>Pharmazie</addtitle><addtitle>Pharmazie</addtitle><description>Objective: Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced
platelet aggregation. Methods: Caffeic acid phenethyl ester (CAPE) is an active component in propolis. CAPE-NO2 is a nitro derivative of CAPE. Its effects on rat platelet aggregation induced by collagen were tested in vitro and the potential mechanisms underlying the
activities were investigated. Results: CAPE-NO2 significantly inhibited collagen-induced platelet aggregation in a concentration-dependent manner. It also reduced TXB2 formation and COX-1 activity in collagen-activated platelets. Moreover, CAPE-NO2 caused
an increase in NO production and cGMP levels and attenuated 5-HT release in the collagen-activated platelets. Conclusion: These findings suggest that the inhibitory mechanism of CAPE-NO2 on collagen-induced platelet aggregation might be associated with the down-regulation
of TXB2, COX-1 and 5-HT and the elevation of NO and cGMP production. These indicators are closely related to platelet function. So CAPE-NO2 may be a promising candidate for the extension of the current spectrum of antiplatelet drugs.</description><subject>Animals</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - metabolism</subject><subject>Caffeic Acids - chemical synthesis</subject><subject>Caffeic Acids - chemistry</subject><subject>Caffeic Acids - pharmacology</subject><subject>Collagen - antagonists & inhibitors</subject><subject>Collagen - pharmacology</subject><subject>Cyclic AMP - biosynthesis</subject><subject>Cyclooxygenase 1 - biosynthesis</subject><subject>In Vitro Techniques</subject><subject>Indicators and Reagents</subject><subject>Male</subject><subject>Nitric Oxide - blood</subject><subject>Phenylethyl Alcohol - analogs & derivatives</subject><subject>Phenylethyl Alcohol - chemical synthesis</subject><subject>Phenylethyl Alcohol - chemistry</subject><subject>Phenylethyl Alcohol - pharmacology</subject><subject>Platelet Aggregation - drug effects</subject><subject>Platelet Aggregation Inhibitors - chemical synthesis</subject><subject>Platelet Aggregation Inhibitors - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Serotonin - blood</subject><subject>Thromboxane B2 - biosynthesis</subject><issn>0031-7144</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kb1vFDEQxV2ASEjoqJFLmr34e-3ydASIFEEKUlte27vnyOdd1t6Tkr8eb-6QaHAzT57nnzxvAPiI0QYLhW-m_YYgzDZUtegNuESI4qbFjF2A9zk_IUQEEfIduCAcc8lbegn6LdxtH26hSSaOw-KhyTCNRx_rTQlTNMVHX6AZfCrQ932woar4DEPahy6UDO0Y49puQnKL9Q7-82iY_WBKGNM1eNubmP2Hc70Cj19vf-2-N_c_v93ttvdNoIyWBhPWUYU4coi3sidWEMLbznaUd1Jw54W3DivmnOkRw14y1akO90ZaaqVg9Ap8PnGnefy9-Fz0IWTr6w-TH5esMa9zEyqZqNZPZ-vSHbzT0xwOZn7Wf7Ophi8nQ0jr9EY_jctcY8p6GI9BT3szH8yLXgPX6PUIdRZIajOXVaiK-fEfTLAn0rqmdUv6KFSSFUgwkphqjJHSzvdmiUUXM-vhRWdF_wBthZS2</recordid><startdate>20140801</startdate><enddate>20140801</enddate><creator>Zhou, Kai</creator><creator>Li, Xiaoli</creator><creator>Du, Qin</creator><creator>Li, Defeng</creator><creator>Hu, Mo</creator><creator>Yang, Xiaojia</creator><creator>Jiang, Qi</creator><creator>Li, Zhubo</creator><general>Govi-Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20140801</creationdate><title>A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation</title><author>Zhou, Kai ; Li, Xiaoli ; Du, Qin ; Li, Defeng ; Hu, Mo ; Yang, Xiaojia ; Jiang, Qi ; Li, Zhubo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i343t-124b39050d0578f2c62257bcb35b865de6ecd194ddaf041e849b9b1fa8c3c8643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - metabolism</topic><topic>Caffeic Acids - chemical synthesis</topic><topic>Caffeic Acids - chemistry</topic><topic>Caffeic Acids - pharmacology</topic><topic>Collagen - antagonists & inhibitors</topic><topic>Collagen - pharmacology</topic><topic>Cyclic AMP - biosynthesis</topic><topic>Cyclooxygenase 1 - biosynthesis</topic><topic>In Vitro Techniques</topic><topic>Indicators and Reagents</topic><topic>Male</topic><topic>Nitric Oxide - blood</topic><topic>Phenylethyl Alcohol - analogs & derivatives</topic><topic>Phenylethyl Alcohol - chemical synthesis</topic><topic>Phenylethyl Alcohol - chemistry</topic><topic>Phenylethyl Alcohol - pharmacology</topic><topic>Platelet Aggregation - drug effects</topic><topic>Platelet Aggregation Inhibitors - chemical synthesis</topic><topic>Platelet Aggregation Inhibitors - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Serotonin - blood</topic><topic>Thromboxane B2 - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Kai</creatorcontrib><creatorcontrib>Li, Xiaoli</creatorcontrib><creatorcontrib>Du, Qin</creatorcontrib><creatorcontrib>Li, Defeng</creatorcontrib><creatorcontrib>Hu, Mo</creatorcontrib><creatorcontrib>Yang, Xiaojia</creatorcontrib><creatorcontrib>Jiang, Qi</creatorcontrib><creatorcontrib>Li, Zhubo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Pharmazie</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Kai</au><au>Li, Xiaoli</au><au>Du, Qin</au><au>Li, Defeng</au><au>Hu, Mo</au><au>Yang, Xiaojia</au><au>Jiang, Qi</au><au>Li, Zhubo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation</atitle><jtitle>Pharmazie</jtitle><stitle>Pharmazie</stitle><addtitle>Pharmazie</addtitle><date>2014-08-01</date><risdate>2014</risdate><volume>69</volume><issue>8</issue><spage>615</spage><epage>620</epage><pages>615-620</pages><issn>0031-7144</issn><abstract>Objective: Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced
platelet aggregation. Methods: Caffeic acid phenethyl ester (CAPE) is an active component in propolis. CAPE-NO2 is a nitro derivative of CAPE. Its effects on rat platelet aggregation induced by collagen were tested in vitro and the potential mechanisms underlying the
activities were investigated. Results: CAPE-NO2 significantly inhibited collagen-induced platelet aggregation in a concentration-dependent manner. It also reduced TXB2 formation and COX-1 activity in collagen-activated platelets. Moreover, CAPE-NO2 caused
an increase in NO production and cGMP levels and attenuated 5-HT release in the collagen-activated platelets. Conclusion: These findings suggest that the inhibitory mechanism of CAPE-NO2 on collagen-induced platelet aggregation might be associated with the down-regulation
of TXB2, COX-1 and 5-HT and the elevation of NO and cGMP production. These indicators are closely related to platelet function. So CAPE-NO2 may be a promising candidate for the extension of the current spectrum of antiplatelet drugs.</abstract><cop>Germany</cop><pub>Govi-Verlag</pub><pmid>25158573</pmid><doi>10.1691/ph.2014.3970</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Blood Platelets - drug effects Blood Platelets - metabolism Caffeic Acids - chemical synthesis Caffeic Acids - chemistry Caffeic Acids - pharmacology Collagen - antagonists & inhibitors Collagen - pharmacology Cyclic AMP - biosynthesis Cyclooxygenase 1 - biosynthesis In Vitro Techniques Indicators and Reagents Male Nitric Oxide - blood Phenylethyl Alcohol - analogs & derivatives Phenylethyl Alcohol - chemical synthesis Phenylethyl Alcohol - chemistry Phenylethyl Alcohol - pharmacology Platelet Aggregation - drug effects Platelet Aggregation Inhibitors - chemical synthesis Platelet Aggregation Inhibitors - pharmacology Rats Rats, Sprague-Dawley Serotonin - blood Thromboxane B2 - biosynthesis |
| title | A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation |
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