지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.1
- 수록면
- 76 - 85 (10page)
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초록· 키워드
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Background: Binding of adhesive proteins (i.e., fibrinogen, fibronectin, vitronectin) to platelet integrin glycoprotein IIb/IIIa (aIIb/β<SUB>3</SUB>) by various agonists (thrombin, collagen, adenosine diphosphate) involve in strength of thrombus. This study was carried out to evaluate the antiplatelet effect of total saponin from Korean Red Ginseng (KRG-TS) by investigating whether KRG-TS inhibits thrombin-induced binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB>.
Methods: We investigated the effect of KRG-TS on phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and dephosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt, affecting binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB>, and clot retraction.
Results: KRG-TS had an antiplatelet effect by inhibiting the binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB> via phosphorylation of VASP (Ser<SUP>157</SUP>), and dephosphorylation of PI3K and Akt on thrombin-induced platelet aggregation. Moreover, A-kinase inhibitor Rp-8-Br-cyclic adenosine monophosphates (cAMPs) reduced KRG-TS-increased VASP (Ser<SUP>157</SUP>) phosphorylation, and increased KRG-TS-inhibited fibrinogen-, and fibronectin-binding to αIIb/β<SUB>3</SUB>. These findings indicate that KRG-TS interferes with the binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB> via cAMP-dependent phosphorylation of VASP (Ser<SUP>157</SUP>). In addition, KRG-TS decreased the rate of clot retraction, reflecting inhibition of αIIb/β<SUB>3</SUB> activation. In this study, we clarified ginsenoside Ro (G-Ro) in KRG-TS inhibited thrombin-induced platelet aggregation via both inhibition of [Ca<SUP>2+</SUP>]i mobilization and increase of cAMP production.
Conclusion: These results strongly indicate that KRG-TS is a beneficial herbal substance inhibiting fibrinogen-, and fibronectin-binding to αIIb/β<SUB>3</SUB>, and clot retraction, and may prevent platelet αIIb/β<SUB>3</SUB>-mediated thrombotic disease. In addition, we demonstrate that G-Ro is a novel compound with antiplatelet characteristics of KRG-TS.
Methods: We investigated the effect of KRG-TS on phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and dephosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt, affecting binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB>, and clot retraction.
Results: KRG-TS had an antiplatelet effect by inhibiting the binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB> via phosphorylation of VASP (Ser<SUP>157</SUP>), and dephosphorylation of PI3K and Akt on thrombin-induced platelet aggregation. Moreover, A-kinase inhibitor Rp-8-Br-cyclic adenosine monophosphates (cAMPs) reduced KRG-TS-increased VASP (Ser<SUP>157</SUP>) phosphorylation, and increased KRG-TS-inhibited fibrinogen-, and fibronectin-binding to αIIb/β<SUB>3</SUB>. These findings indicate that KRG-TS interferes with the binding of fibrinogen and fibronectin to αIIb/β<SUB>3</SUB> via cAMP-dependent phosphorylation of VASP (Ser<SUP>157</SUP>). In addition, KRG-TS decreased the rate of clot retraction, reflecting inhibition of αIIb/β<SUB>3</SUB> activation. In this study, we clarified ginsenoside Ro (G-Ro) in KRG-TS inhibited thrombin-induced platelet aggregation via both inhibition of [Ca<SUP>2+</SUP>]i mobilization and increase of cAMP production.
Conclusion: These results strongly indicate that KRG-TS is a beneficial herbal substance inhibiting fibrinogen-, and fibronectin-binding to αIIb/β<SUB>3</SUB>, and clot retraction, and may prevent platelet αIIb/β<SUB>3</SUB>-mediated thrombotic disease. In addition, we demonstrate that G-Ro is a novel compound with antiplatelet characteristics of KRG-TS.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
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UCI(KEPA) : I410-ECN-0101-2018-524-001598123