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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
- 2015.10
- 수록면
- 354 - 364 (11page)
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초록· 키워드
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Background: Intracellular Ca<SUP>2+</SUP>([Ca<SUP>2+</SUP>]i) is a platelet aggregation-inducing molecule. Therefore, understanding the inhibitory mechanism of [Ca<SUP>2+</SUP>]i mobilization is very important to evaluate the antiplatelet effect of a substance. This study was carried out to understand the Ca<SUP>2+</SUP>-antagonistic effect of total saponin from Korean Red Ginseng (KRG-TS).
Methods: We investigated the Ca<SUP>2+</SUP>-antagonistic effect of KRG-TS on cyclic nucleotides-associated phosphorylation of inositol 1,4,5-trisphosphate receptor type I (IP₃RI) and cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) in thrombin (0.05 U/mL)-stimulated human platelet aggregation.
Results: The inhibition of [Ca<SUP>2+</SUP>]i mobilization by KRG-TS was increased by a PKA inhibitor (Rp-8-BrcAMPS), which was more stronger than the inhibition by a cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG) inhibitor (Rp-8-Br-cGMPS). In addition, Rp-8-Br-cAMPS inhibited phosphorylation of PKA catalytic subunit (PKAc) (Thr<SUP>197</SUP>) by KRG-TS. The phosphorylation of IP₃RI (Ser<SUP>1756</SUP>) by KRG-TS was very strongly inhibited by Rp-8-Br-cAMPS compared with that by Rp-8-BrcGMPS. These results suggest that the inhibitory effect of [Ca<SUP>2+</SUP>]i mobilization by KRG-TS is more strongly dependent on a cAMP/PKA pathway than a cGMP/PKG pathway. KRG-TS also inhibited the release of adenosine triphosphate and serotonin. In addition, only G-Rg3 of protopanaxadiol in KRG-TS inhibited thrombin-induced platelet aggregation.
Conclusion: These results strongly indicate that KRG-TS is a potent beneficial compound that inhibits [Ca<SUP>2+</SUP>]i mobilization in thrombineplatelet interactions, which may result in the prevention of platelet aggregation-mediated thrombotic disease.
Methods: We investigated the Ca<SUP>2+</SUP>-antagonistic effect of KRG-TS on cyclic nucleotides-associated phosphorylation of inositol 1,4,5-trisphosphate receptor type I (IP₃RI) and cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) in thrombin (0.05 U/mL)-stimulated human platelet aggregation.
Results: The inhibition of [Ca<SUP>2+</SUP>]i mobilization by KRG-TS was increased by a PKA inhibitor (Rp-8-BrcAMPS), which was more stronger than the inhibition by a cyclic guanosine monophosphate (cGMP)-dependent protein kinase (PKG) inhibitor (Rp-8-Br-cGMPS). In addition, Rp-8-Br-cAMPS inhibited phosphorylation of PKA catalytic subunit (PKAc) (Thr<SUP>197</SUP>) by KRG-TS. The phosphorylation of IP₃RI (Ser<SUP>1756</SUP>) by KRG-TS was very strongly inhibited by Rp-8-Br-cAMPS compared with that by Rp-8-BrcGMPS. These results suggest that the inhibitory effect of [Ca<SUP>2+</SUP>]i mobilization by KRG-TS is more strongly dependent on a cAMP/PKA pathway than a cGMP/PKG pathway. KRG-TS also inhibited the release of adenosine triphosphate and serotonin. In addition, only G-Rg3 of protopanaxadiol in KRG-TS inhibited thrombin-induced platelet aggregation.
Conclusion: These results strongly indicate that KRG-TS is a potent beneficial compound that inhibits [Ca<SUP>2+</SUP>]i mobilization in thrombineplatelet interactions, which may result in the prevention of platelet aggregation-mediated thrombotic disease.
목차
abstract
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
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UCI(KEPA) : I410-ECN-0101-2018-524-001597944