title: A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation.
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.
  
  
  CONCLUSIONS
  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.
authors.forename: Kai
authors.initials: K
authors.lastname: Zhou
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Li
authors.forename: Qin
authors.initials: Q
authors.lastname: Du
authors.forename: Defeng
authors.initials: D
authors.lastname: Li
authors.forename: Mo
authors.initials: M
authors.lastname: Hu
authors.forename: Xiaojia
authors.initials: X
authors.lastname: Yang
authors.forename: Qi
authors.initials: Q
authors.lastname: Jiang
authors.forename: Zhubo
authors.initials: Z
authors.lastname: Li
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D002109:Caffeic Acids / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology*; D003094:Collagen / Q000037:antagonists & inhibitors* / Q000494:pharmacology*; D000242:Cyclic AMP / Q000096:biosynthesis; D051545:Cyclooxygenase 1 / Q000096:biosynthesis; D066298:In Vitro Techniques; D007202:Indicators and Reagents; D008297:Male; D009569:Nitric Oxide / Q000097:blood; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000138:chemical synthesis* / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000097:blood; D013929:Thromboxane B2 / Q000096:biosynthesis
chemical_list: D002109:Caffeic Acids; D007202:Indicators and Reagents; D010975:Platelet Aggregation Inhibitors; D009569:Nitric Oxide; D012701:Serotonin; D013929:Thromboxane B2; D003094:Collagen; D000242:Cyclic AMP; D051545:Cyclooxygenase 1; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol