• Korean Journal of Veterinary Research
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• v.55 no.4
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• pp.233-240
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• 2015

Although the effects of the rice bran have recently been investigated, there is no information regarding platelet physiology available. However, it is well known that fermented natural plants have a beneficial effect on cardiovascular diseases. Therefore, this study was conducted to investigate whether fermented rice bran extract (FRBE) with several plants (Artemisia princeps, Angelica Gigantis Radix, Cnidium officinale, and Camellia sinensis) affected agonist-induced platelet aggregation, and if so, what the underlying mechanism of its activity was. We performed several experiments, including in vitro platelet aggregation, intracellular calcium concentration and adenosine triphosphate release. In addition, the activation of integrin ${\alpha}_{II}b{\beta}3$ was determined using fibrinogen binding. Thrombus formation was also evaluated in vivo using an arterio-venous shunt model. The FRBE inhibited collagen-induced platelet aggregation in a concentration-dependent manner. FRBE significantly and dose dependently attenuated thrombus formation using rat arterio-venous shunt. FRBE suppressed the intracellular calcium mobilization in collagen-stimulated platelets. We also found that FRBE inhibited extracellular stimuli-responsive kinase 1/2, p38-mitogen-activated protein kinases and c-Jun N-terminal kinase phosphorylation. These results suggested that FRBE inhibited collagen-induced platelet aggregation, which was mediated by modulation of downstream signaling molecules. In conclusion, FRBE could be developed as a functional food against aberrant platelet activation-related cardiovascular diseases.

• Journal of Ginseng Research
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• v.41 no.1
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• pp.96-102
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• 2017

Background: Korean ginseng, Panax ginseng Meyer, has been used as a traditional oriental medicine to treat illness and promote health for several thousand years. Ginsenosides are the main constituents for the pharmacological effects of P. ginseng. Since several ginsenosides, including ginsenoside (G)-Rg3 and G-Rp1, have reported antiplatelet activity, here we investigate the ability of G-Rp4 to modulate adenosine diphosphate (ADP)-induced platelet aggregation. The ginsenoside Rp4, a similar chemical structure of G-Rp1, was prepared from G-Rg1 by chemical modification. Methods: To examine the effects of G-Rp4 on platelet activation, we performed several experiments, including antiplatelet ability, the modulation of intracellular calcium concentration, and P-selectin expression. In addition, we examined the activation of integrin ${\alpha}IIb{\beta}_3$ and the phosphorylation of signaling molecules using fibrinogen binding assay and immunoblotting in rat washed platelets. Results: G-Rp4 inhibited ADP-induced platelet aggregation in a dose-dependent manner. We found that G-Rp4 decreased calcium mobilization and P-selectin expression in ADP-activated platelets. Moreover, fibrinogen binding to integrin ${\alpha}IIb{\beta}_3$ by ADP was attenuated in G-Rp4-treated platelets. G-Rp4 significantly attenuated phosphorylation of extracellular signal-regulated protein kinases 1 and 2, p38, and c-Jun N-terminal kinase, as well as protein kinase B, phosphatidylinositol 3-kinase, and phospholipase C-${\gamma}$ phosphorylations. Conclusion: G-Rp4 significantly inhibited ADP-induced platelet aggregation and this is mediated via modulating the intracellular signaling molecules. These results indicate that G-Rp4 could be a potential candidate as a therapeutic agent against platelet-related cardiovascular diseases.

• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.208.1-208
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• 2001

No Abstract, See Full Text

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2005.10a
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• pp.63-64
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• 2005

• Proceedings of the Microbiological Society of Korea Conference
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• 2009.05a
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• pp.139-140
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• 2009

• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.120.2-120.2
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• 2006

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.86-87
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• 2000

• Journal of Medicine and Life Science
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• v.20 no.3
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• pp.135-138
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• 2023

• Journal of Life Science
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• v.16 no.3 s.76
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• pp.433-441
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• 2006

Polyamines are essential for the normal cell growth and differentiation. They are also known to have paradoxical dual effects on cell proliferation. In this paper we show that the excess amount of polyamines induces apoptosis through the modulation of calcium signaling in LNCaP human prostate cancer cells. Polyamines, particularly spermidine and spermine, stimulated cell proliferation at a lower concentration (under 10 ${\mu}M$), but it inhibited cell viability at a higher concentration (40 ${\mu}M$). The levels of intracellular $Ca^{2+}$ concentration were increased only at a high concentration of polyamines treatment without any noticeable changes at lower concentrations. Nifedipine did not alter the increase of polyamine-induced $Ca^{2+}$ levels, but flufenamic acid totally abolished the increase of intracellular $Ca^{2+}$ levels. These results mean that polyamines induce $Ca^{2+}$ influx from the surroundings through nonselective cation channels on the cell membrane. The expression of Bcl-2 protein was almost completely blocked, but the level of Bax protein was increased dramatically in the cells treated with high concentration of polyamine. The present study shows that polyamines at a high concentration induce apoptosis through the modulation of intracellular calcium signaling. The increase of intracellular calcium level induced by polyamines, was possibly a result from the extracellular calcium influx through the nonselective cation channels.

• Development and Reproduction
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• v.15 no.1
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• pp.17-24
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• 2011

Lipid metabolites involved in cellular regulation as signaling mediators. Prostaglandins (PGs), metabolites of lipid are involved to pregnancy at the time of implantation but the functional roles of PGs on embryo development are still controversy and largely unknown. In previous report, the levels of $PGE_2$ and $PGF_{2a}$ at embryos of morula stage and blastocyst stage were explored (Cheon et al., 1998). In this study, the previous suggestion was confirmed and the possible downstream mediator of prostaglandin $E_2$ and prostaglandin $F_{2a}$ on the expansion and hatching of mouse embryo was examined. As expected, developmental rate of the blastocyst to expanded stage was a concentration-response curve that showed the highest expansion rate at 10 ${\mu}M$ $PGE_2$, but at 100 ${\mu}M$ $PGE_2$, the rate was decreased. In contrast to the $PGE_2$, $PGF_{2a}$ stimulated expansion without toxicity at highest concentration. Cotreatment of PGs with indomethacin overcame the inhibitory effects of indomethacin in expansion. Exogenous PGs also improved the development of expanded embryos to the hatching stage. Besides, PGs receptors' transcripts detected at blastocyst. $PGE_2$ was caused of calcium fluctuation in the blastocyst but $PGF_{2a}$ did not. The changes of intracellular calcium concentration were different between indomethacin pretreated embryos and non-treated embryos. Based on these results it is suggested that PGs work as paracrine and/or autocrine factors through calcium and the others which were not identified in this study.