Abstract
This study aimed to investigate the effect of polydatin against thrombosis and its possible mechanisms. The methods of injection of arachidonic acid into mouse tail vein electrically stimulated carotid thrombosis in rats, and the rats’ inferior vena ligation were used to evaluate the antithrombotic effects of polydatin. Platelet aggregation was tested by use of Born’s method, and platelet cytosolic calcium was determined by use of Fura-2/AM. Thromboxane B2 and 6-keto-prostaglandin F1α level was monitored by the immuno-assay, while Rosette assay and Born’s method were used to observe platelet-neutrophil interactions. The results show that polydatin had evident antithrombotic effects in the multiple-thrombosis models; the mechanisms may be closely related to its anti-platelet aggregation, which results in decrease of platelet cytosolic calcium and plasma thromboxane B2, while increasing plasma 6-keto-prostaglandin F1α Level and suppressing of platelet-neutrophil interactions. Key words: Polydatin, thromboxane A2, prostacyclin, platelet, neutrophil, cytosolic calcium.
Highlights
Modern researches show that the process of thrombosis is closely related with interactions of platelets, leukocytes and other cells
The results show that polydatin had evident antithrombotic effects in the multiple-thrombosis models; the mechanisms may be closely related to its anti-platelet aggregation, which results in decrease of platelet cytosolic calcium and plasma thromboxane B2, while increasing plasma 6-keto-prostaglandin F1 Level and suppressing of platelet-neutrophil interactions
It is suggested that polydatin showed potent inhibition on the activity of Arachidonic acid (AA) and thromboxane A2 (TXA2)
Summary
Modern researches show that the process of thrombosis is closely related with interactions of platelets, leukocytes and other cells. Activated platelets can release some active substances including platelet activating factor (PAF) and thromboxane. Such active substances activate polymorphonuclear leukocytes (PMN), and activated PMNs accelerate the expression of platelet selectin so that adhesion between PMNs and platelets occurs while producing more thromboxane and promoting the mobilization of platelet intracellular calcium (Armstrong et al, 2008; Chlopicki et al, 2003). An obvious platelet aggregation is induced, which results in acceleration of the process of thrombosis eventually. Thromboembolic diseases are great threats to human’s life and health and prevention and treatment of thrombosis is a focus of modern medical research.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
