期刊
JOURNAL OF GINSENG RESEARCH
卷 35, 期 2, 页码 191-199出版社
KOREAN SOC GINSENG
DOI: 10.5142/jgr.2011.35.2.191
关键词
Panax ginseng; Ginsenoside metabolites; Human ether-a-go-go-related gene K+ channel; Human heart
资金
- Korea Ginseng Corporation
- Ministry of Education, Science and Technology [2009-0093824]
- BK21
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 cardio-protective effects. In a previous report we demonstrated that ginsenoside Rg(3) 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 alpha subunits in Xenopus oocytes. CK induced a large persistent deactivating-tail current (Ideactivating-tail) and significantly decelerated deactivating current decay in a concentration-dependent manner. The EC50 for persistent Ideactivating-tail was 16.6 +/- 1.3 mu M. In contrast to CK, PPT accelerated deactivating-tail current deactivation. PPD itself had no effects on deactivating-tail currents, whereas PPD inhibited ginsenoside Rg(3)-induced persistent Ideactivating-tail and accelerated HERG K+ channel deactivation in a concentration-dependent manner. These results indicate that ginsenoside metabolites exhibit differential regulation on Ideactivating-tail of HERG K+ channel.
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