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자료유형
학술저널
저자정보
Cho, Hyun-Jeong (Department of Biomedical Laboratory Science, College of Medical Science, Konyang University) Choi, Sun-A (Department of Biomedical Laboratory Science, College of Biomedical Science, Inje University) Kim, Chun-Gyu (Department of Pharmaceutical Engineering, College of Engineering, Inje University) Jung, Tae-Sung (Department of Pharmacy, Kungsung University) Hong, Jeong-Hwa (School of Food and Life Science, College of Biomedical Science and Engineering, Inje University) Rhee, Man-Hee (College of Veterinary Medicine, Kyungpook National University) Park, Hye-Jin (Department of Bioscience and Biotechnology, Konkuk University) Park, Hwa-Jin (Department of Biomedical Laboratory Science, College of Biomedical Science, Inje University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제2호
발행연도
2011.1
수록면
218 - 223 (6page)

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In this study, we investigated the effect of spinach saponin-enriched fraction (SSEF) on collagen (10 ${\mu}g/ml$)-stimulated platelet aggregation. SSEF inhibited collagen-induced platelet aggregation, and which was involved in the inhibition of thromboxane $A_2$ ($TXA_2$) production, an intracellular $Ca^{2+}$-agonist as an aggregation-inducing autacoidal molecule. In addition, SSEF significantly increased the formation of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), intracellular $Ca^{2+}$-antagonists as aggregation-inhibiting molecules, in collagen-stimulated platelets. These results suggest that SSEF might inhibit $Ca^{2+}$-elevation and $TXA_2$ formation by increasing the production of $Ca^{2+}$-antagonistic molecules cAMP and cGMP. These mean that SSEF is a potent inhibitor of collagen-stimulated platelet aggregation. On the other hand, prothrombin time (PT) and activated partial thromboplastin time (APTT) were potently prolonged by SSEF. These findings suggest that SSEF prolongs the internal time between the conversion of fibrinogen to fibrin. Accordingly, our data demonstrate that SSEF may be a crucial tool for a negative regulator during platelet activation and blood coagulation on thrombotic diseases.

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