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Ikuo Saiki 고려인삼학회 2007 Journal of Ginseng Research Vol.31 No.1
We found that the main bacterial metabolite M1 is an active component of orally administered protopanxadioltype ginsenosides, and that the anti-metastatic effect by oral administration of ginsenosides may be primarily mediated through the inhibition of tumor invasion, migration and growth of tumor cells by their metabolite M1. Pharmacokinetic study after oral administration of ginsenoside Rb1 revealed that M1 was detected in serum for 24 h by HPLC analysis but Rb1 was not detected. M1, with anti-metastatic property, inhibited the proliferation of murine and human tumor cells in a time- and concentration-dependent manner in vitro, and also induced apoptotic cell death (the ladder fragmentation of the extracted DNA). The induction of apoptosis by M1 involved the up-regulation of the cyclin-dependent kinase (CDK) inhibitor p27<SUP>Kip1</SUP> as well as the down-regulation of a proto-oncogene product c-Myc and cyclin D1 in a timedependent manner. Thus, M1 might cause the cell-cycle arrest (G1 phase arrest) in tumor cells through the up/down-regulation of these cell-growth related molecules, and consequently induce apoptosis. The nucleosomal distribution of fluorescence- labeled M1 suggests that the modification of these molecules is induced by transcriptional regulation. Tumorinduced angiogenesis (neovascularization) is one of the most important events concerning tumor growth and metastasis. Neovascularization toward and into tumor is a crucial step for the delivery of nutrition and oxygen to tumors, and also functions as the metastatic pathway to distant organs. M1 inhibited the tube-like formation of hepatic sinusoidal endothelial (HSE) cells induced by the conditioned medium of colon 26-L5 cells in a concentration-dependent manner. However, M1 at the concentrations used in this study did not affect the growth of HSE cells in vitro.
Saiki, Ikuo 경희대학교 2001 INTERNATIONAL SYMPOSIUM ON EAST-WEST MEDICINE Vol.2001 No.1
Ginseng(the root of Panax ginseng C. A. MEYER, Araliaceae) has been used for traditional medicine in China, Korea, Japan and other Asian countries for the treatment of various diseases including psychiatric and neurologic diseases as well as diabetes mellitus. So far, ginseng saponins(ginsenosides) have been regarded as the principal componentsresponsible for the pharmacological activities of ginseng. Previously, it was reported thatprotopanaxadiol-type ginsenisides such as Rb1, Rb2 and Rc are metabolized by intestinalbacteria after oral administration to their final derivative 20-O-b-D-glucopyranosyl-20(S)-protopanaxadiol, which is referred to as M1 or compound K. In the present study, we investigated in vivo and in vitro anti-metastatic activities of M1 in comparison with ginsenosides Rb1, Rb2 and Rc and its inhibitory mechanism of action. The main bacterial metabolite M1 is an active component of orally administered ginsenosides, and that the anti-metastatic effect by oral administration of ginsenosides may be primarily mediated through the inhibition of tumor invasion, migration and growth of tumor cells by their metabolite M1. M1 inhibited the proliferation of tumor cells in a time-and concentration-dependent manner, and in addition induced apoptotic cell death. The induction of apoptosis by M1 involved the up-regulation of the CDK-inhibtor p27kipl as well as the down-regulation of c-Myc and cyclic D1. The nucleosomal distribution of M1 suggests that the modification of these molecules is induced by transcriptional regulation.
Saiki, Ikuo The Korean Society of Ginseng 2007 Journal of Ginseng Research Vol.31 No.1
We found that the main bacterial metabolite M1 is an active component of orally administered protopanxadiol-type ginsenosides, and that the anti-metastatic effect by oral administration of ginsenosides may be primarily mediated through the inhibition of tumor invasion, migration and growth of tumor cells by their metabolite M1. Pharmacokinetic study after oral administration of ginsenoside Rb1 revealed that M1 was detected in serum for 24 h by HPLC analysis but Rb1 was not detected. M1, with anti-metastatic property, inhibited the proliferation of murine and human tumor cells in a time- and concentration-dependent manner in vitro, and also induced apoptotic cell death (the ladder fragmentation of the extracted DNA). The induction of apoptosis by M1 involved the up-regulation of the cyclin-dependent kinase(CDK) inhibitor $p27^{Kip1}$ as well as the down-regulation of a proto-oncogene product c-Myc and cyclin D1 in a time-dependent manner. Thus, M1 might cause the cell-cycle arrest (G1 phase arrest) in honor cells through the up/down-regulation of these cell-growth related molecules, and consequently induce apoptosis. The nucleosomal distribution of fluorescence-labeled M1 suggests that the modification of these molecules is induced by transcriptional regulation. Tumor-induced angiogenesis (neovascularization) is one of the most important events concerning tumor growth and metastasis. Neovascularization toward and into tumor is a crucial step for the delivery of nutrition and oxygen to tumors, and also functions as the metastatic pathway to distant organs. M1 inhibited the tube-like formation of hepatic sinusoidal endothelial (HSE) cells induced by the conditioned medium of colon 26-L5 cells in a concentration-dependent manner. However, M1 at the concentrations used in this study did not affect the growth of HSE cells in vitro.
Saiki, Ikuo,Murata, Jun,Fujii, Hideki,Kato, Toshimitsu The Korean Nutrition Society 2004 Nutritional Sciences Vol.7 No.3
We have investigated the effect of calcium spirulan(Ca-SP) isolated from a blue-green alga Spirulina platensis, which is a sulfated polysaccharide chelating calcium and mainly composed of rhamnose and fructose, on invasion of both B16- BL6 melanoma cells, Colon 26 carcinoma and HT-1080 fibrosarcoma cells through reconstituted basement membrane (Matrigel). Ca-SP significantly inhibited the invasion of these tumor cells through Matrigel/fibronectin-coated filters in a concentration-dependent manner. Ca-SP also inhibited the haptotactic migration of tumor cells to laminin, but it had no inhibitory effect on tumor cell migration to fibronectin-coated filters. Ca-SP prevented the adhesion of B16-BL6 cells to Matrigel- and laminin-substrates but did not affect the adhesion to fibronectin. The pretreatment of tumor cells with Ca-SP inhibited the adhesion to laminin in a concentration-dependent fashion, while the pretreatment of laminin-substrates did not. Ca-SP had no effect on the production and activation of type IV collagenase in gelatin zymography. In contraset, Ca-SP significantly inhibited degradation of heparan sulfate by purified heparanase. The experimental lung metastasis was significantly reduced by co-injection of B16-BL6 cells with Ca-SP in a dose-dependent manner. Seven intermittent ⅰ.ⅴ. injection of 100$\mu\textrm{g}$ of Ca-SP caused a marked decrease of lung tumor colonization of B16-BL6 cells in a spontaneous lung metastasis model. These results suggest that Ca-SP, a novel sulfated polysaccharide, could reduce the lung colonization of B16-BL6 melanoma cells in experimental metastasis model, by inhibiting the tumor invasion of basement membrane Matrigel, probably through the prevention of the adhesion and migration of tumor cells to laminin-substrate and of the heparanase activity.