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(Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University) (Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University) (Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University) (Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University) (Department of Microbiology, College of Medicine and Applied Radiological Science Research Institute, Cheju National University) (Department of Neuro-science, Ewha Womans University Medical School) (Department of Microbial Chemistry, College of Pharmacy, Kyung Hee University) (Department of Microbial Chemistry, College of Pharmacy, Kyung Hee University) (Department of Biochemistry, College of Medicine and Applied Radiological Science Research Institute, Cheju National University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제28권 제6호
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    초록·키워드

    We recently reported that the ginseng saponin metabolite, compound K (20-O-$\beta$-D-glucopyra-nosyl-20(S)-protopanaxadiol, IH901), inhibits the growth of U937 cells through caspase-dependent apoptosis pathway. In this study, we further characterized the effects of compound K on U937 cells and found that, in addition to apoptosis, compound K induced the arrest of the G1 phase. The compound K treated U937 cells showed increased p21 expression; an inhibitory protein of cyclincdk complex. The up-regulation of p21 was followed by the inactivation of cyclin D and the cdk4 protein, which act at the early $G_1$ phase, and cyclin E, which acts at the late $G_1$ phase. Furthermore, compound K induced the activation of JNK and the transcription factor AP-1, which is a downstream target of JNK. These findings suggest that the up-regulation of p21 and activation of JNK in the compound K treated cells contribute to the arrest of the $G_1$ phase.

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