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ORIGINAL ARTICLE
Year : 2020  |  Volume : 5  |  Issue : 1  |  Page : 42-50

Alginate oligosaccharide inhibits platelet activation with minimal impact on bleeding time


1 Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Fudan University, Shanghai, China
2 Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, China

Correspondence Address:
Dr. Jun-Bo Ge
Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Fudan University, Shanghai
China
Prof. Ying-Nan Bai
Department of Cardiology, Zhongshan Hospital, Shanghai Institute of Cardiovascular Diseases, Fudan University, Shanghai
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cp.cp_2_20

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Background: Antiplatelet drugs are widely used in the prevention and treatment of arterial thrombotic diseases but are associated with increased risk of bleeding. Alginate oligosaccharide (AOS), a biodegradable polymer extracted from macroalgae, has been shown to inhibit phosphorylation of mitogen-activated protein kinases, which, in turn, are critical for platelet activation. The present study aimed to examine whether AOS possesses antiplatelet and antithrombotic activity, and if so, the underlying mechanisms. Methods: We detected the effects of AOS on human platelet aggregation and adenosine triphosphate (ATP) release induced by thrombin and collagen, as well as platelet clot retraction and spreading. FeCl3-injured mouse mesenteric arteriole thrombosis was evaluated in adult C57BL/6 mice pretreated with either AOS (200 mg/kg/d through gavage for 7 consecutive days) or clopidogrel (30 mg/kg/d for 2 days). The impact of AOS on bleeding time in comparison to clopidogrel was also analyzed. Results: At a range of 0.1–1.0 mg/mL, AOS concentration dependently inhibited human platelet aggregation and ATP release induced by thrombin and collagen, as well as platelet clot retraction and spreading. The final occlusion time injured by FeCl3in mice pretreated with AOS was significantly increased (from 11.9 ± 0.9 min in vehicle control to 17.6 ± 1.0 min, P < 0.01), as well as the first occlusion time (from 4.4 ± 0.5 min in vehicle control to 7.6 ± 0.7 min, P < 0.01). Bleeding time on tail snip was 534 ± 62 s in vehicle control, 581 ± 60 s in mice with AOS pretreatment (P = 0.59 vs. control), and 1260 ± 83 s in mice receiving clopidogrel pretreatment (P < 0.01 vs. control). Preliminary mechanistic investigation using human platelets showed a decreased level of phosphorylated MAP kinases (i.e., p38, Erk1/2, and JNK) by AOS. Conclusions: AOS has antiplatelet and antithrombotic activity, with minimal impact on bleeding time.


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