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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
- 2011.6
- 수록면
- 191 - 199 (9page)
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The human ether-a-go-go-related gene (HERG) cardiac K? channels are one of the representative pharmacological targets for development of drugs against cardiovascular diseases such as arrhythmia. Panax ginseng has been known to exhibit cardioprotective effects. In a previous report we demonstrated that ginsenoside Rg₃ regulates HERG K? channels by decelerating deactivation. However, little is known about how ginsenoside metabolites regulate HERG K? channel activity. In the present study, we examined the effects of ginsenoside metabolites such as compound K (CK), protopanaxadiol (PPD), and protopanaxatriol (PPT) on HERG K? channel activity by expressing human a subunits in Xenopus oocytes. CK induced a large persistent deactivatingtail current (I<SUB>deactivating-tail</SUB>) and significantly decelerated deactivating current decay in a concentration-dependent manner. The EC?? for persistent I<SUB>deactivating-tail</SUB> was 16.6±1.3 μM. In contrast to CK, PPT accelerated deactivating-tail current deactivation. PPD itself had no effects on deactivating-tail currents, whereas PPD inhibited ginsenoside Rg₃-induced persistent I<SUB>deactivating-tail</SUB> and accelerated HERG K+ channel deactivation in a concentration-dependent manner. These results indicate that ginsenoside metabolites exhibit differential regulation on I<SUB>deactivating-tail</SUB> of HERG K? channel.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES
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