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Oh, Seikwan,Kim, Hack-Seang,Seong, Yeon-Hee The Pharmaceutical Society of Korea 1995 Archives of Pharmacal Research Vol.18 No.5
These studies were designed to examine the effects of ginsenosides on glutamate neurotansmission. In primary cultures of rat cerebellar granule cells, ginsenosides (Rb1, Rc did not Rg1, $500\mug/ml$) increased glutamate release which was measured by HPLC. but HPLC, but Re did not shwo an elevation of glutamate release. However, all of these ginsenosides down-regulated N-methyl-D-aspartate (NMDA)-induced glutamate release. Rc strongly increased glutamate release and elevated intracellular clcium concentrations $([Ca_{2+}]_i)$ which was measured by ratio fluorometry with FURA-2AM. These results indicate that ginsenosides have a homeostatic effect on glutamate neurotransmission, and there is a structure-function relationship among the ginsenosides tested.
Oh, Seikwan,Moon, Hyung-In,Jung, Jae-Chul,Avery, Mitchell A. Walter de Gruyter GmbH 2008 Zeitschrift für Naturforschung. B, A journal Vol.63 No.11
<B>Abstract</B><P> A simple synthesis, involving a key coupling reaction, and the biological activity of the title compounds 16 and 17 are described. The key fragments are the amine·HCl salt 6 and the acids 9 and 13, which were smoothly coupled by using ethyl(dimethylaminopropyl)carbodiimide (EDCI) and 1- hydroxybenzotriazole (HOBt) in high yield.We have found that the in vitro growth inhibitory potency of the new compounds 16 and 17 exhibits good histone deacetylase (HDAC) activity.</P>
Changes of the Level of G Protein α-subunit mRNA by Withdrawal from Morphine and Butorphanol
Seikwan Oh 대한생리학회-대한약리학회 2000 The Korean Journal of Physiology & Pharmacology Vol.4 No.4
<P> Morphine or butorphanol was continuously infused into cerebroventricle (i.c.v.) with the rate of 26 nmol/ μl/h for 3 days, and the withdrawal from opioid was rendered 7 hrs after the stopping of infusion. The expression of physical dependence produced by these opioids was evaluated by measuring the naloxone- precipitated withdrawal signs. The withdrawal signs produced in animals dependent on butorphanol (<I>kappa</I> opioid receptor agonist) were similar to those of morphine (<I>mu</I> opioid receptor agonist). Besides the behavioral modifications, opioid withdrawal affected G protein expression in the central nervous system. The G-protein α-subunit has been implicated in opioid tolerance and withdrawal. The effects of continuous infusion of morphine or butorphanol on the modulation of G protein α-subunit mRNA were investigated by using in situ hybridization study. In situ hybridization showed that the levels of Gαs and Gαi were changed during opioid withdrawal. Specifically, the level of Gαs mRNA was decreased in the cortex and cerebellar granule layer during the morphine and butorphanol withdrawal. The level of Gαi mRNA was decreased in the dentate gyrus and cerebellar granule layer during the morphine withdrawal. However, the level of Gαi mRNA was significantly elevated during the butorphanol withdrawal. These results suggest that region-specific changes of G protein α-subunit mRNA were involved in the withdrawal from morphine and butorphanol.
오세관(Seikwan Oh) 고려인삼학회 2008 Journal of Ginseng Research Vol.32 No.1
Ginseng saponin has been shown to inhibit the development of dependence on morphine, cocaine, methamphetamine, but the antinarcotics effects of ginseng on nalbuphine remains still largely unknown. Ginseng administration attenuated the naloxone-induced jumping behavior on nalbuphine dependent mice. The development of morphine dependence was mediated through μ-opioid receptor, however, development of nalbuphine dependence was mediated through κ-opioid receptor. However, it was found that the efficacy of analgesic antagonism of GTS was mediated through the serotonergic mechanism, not mediated through the opioid receptor. In addition, ginseng administration modulated cellular signal transduction in the brain. The increased NMDA receptor subunit (NR1, pNR1), phosphate extracellular signal regulated protein kinase (pERK), phosphate cAMP response element binding protein (pCREB) expression by nalbuphine was decreased by the administration of ginseng powder in cortex, hippocampus, striatum of rat brain. These results suggest that ginseng could be one of the targets of antinarcotic therapies to reduce the development of tolerance and dependence on nalbuphine as well as morphine.
Shin, Kyong-Oh,Seo, Cho-Hee,Cho, Hyo-Hyun,Oh, Seikwan,Hong, Seon-Pyo,Yoo, Hwan-Soo,Hong, Jin-Tae,Oh, Ki-Wan,Lee, Yong-Moon 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.9
Ginsenoside compound K (CK) is a metabolite of the protopanaxadiol-type saponins of Panax ginseng C.A. Meyer (Araliaceae), has long been used to treat against the development of cancer, inflammation, allergies, and diabetes. This study examined the anti-angiogenic properties of CK against sphingosine 1-phosphate (S1P)-induced cell migration via regulation of sphingosine kinase 1 (SPHK1) in human umbilical vein endothelial cells (HUVEC). Studies on S1P-induced cell migration, expression of SPHK1 and MMPs and analysis of sphingolipidmetabolites by LC-MS/MS were examined after the treatment of CK (2.5, 5, $10{\mu}g/mL$) in HUVEC. S1P produced by SPHK1 is also involved in cell growth, migration, and protection of apoptosis; therefore, we sought to investigate whether ginsenosides are able to regulate SPHK1. For this purpose, we developed an inhibitory assay of SPHK1 activity and an analytical method for detection of S1P and other sphingolipid metabolites in HUVEC. Ginsenoside CK inhibited 100 nM S1P-induced cell migrations in a dose-dependent manner. Among tested ginsenosides, CK exclusively inhibited S1P production, SPHK1 activity and SPHK1 expression in HUVEC, whereas expression of the pro-apoptotic sphingolipids, sphingosine and ceramide, was increased in response to CK. The major subspecies of the increased ceramide was C24:0-ceramide. CKalso disrupted the sphingolipid rheostat, which ultimately influences cell fate, and dose-dependently inhibited HUVEC migration by reducing expression of metalloproteinases (MMPs). Ginsenoside CK acts as a unique HUVEC migration inhibitor by regulating MMP expression, as well as the activity of SPHK1 and its related sphingolipid metabolites.
Choi, Shinkyu,Kim, Ji Aee,Li, Hai‐,yan,Shin, Kyong‐,Oh,Oh, Goo Taeg,Lee, Yong‐,Moon,Oh, Seikwan,Pewzner‐,Jung, Yael,Futerman, Anthony H.,Suh, Suk Hyo BLACKWELL PUBLISHING 2016 AGING CELL Vol.15 No.5
<P><B>Summary</B></P><P>Endothelial oxidative stress develops with aging and reactive oxygen species impair endothelium‐dependent relaxation (EDR) by decreasing nitric oxide (NO) availability. Endothelial K<SUB>Ca</SUB>3.1, which contributes to EDR, is upregulated by H<SUB>2</SUB>O<SUB>2</SUB>. We investigated whether K<SUB>Ca</SUB>3.1 upregulation compensates for diminished EDR to NO during aging‐related oxidative stress. Previous studies identified that the levels of ceramide synthase 5 (CerS5), sphingosine, and sphingosine 1‐phosphate were increased in aged wild‐type and CerS2 mice. In primary mouse aortic endothelial cells (MAECs) from aged wild‐type and CerS2 null mice, superoxide dismutase (SOD) was upregulated, and catalase and glutathione peroxidase 1 (GPX1) were downregulated, when compared to MAECs from young and age‐matched wild‐type mice. Increased H<SUB>2</SUB>O<SUB>2</SUB> levels induced Fyn and extracellular signal‐regulated kinases (ERKs) phosphorylation and K<SUB>Ca</SUB>3.1 upregulation. Catalase/GPX1 double knockout (catalase<SUP>−/−</SUP>/GPX1<SUP>−/−</SUP>) upregulated K<SUB>Ca</SUB>3.1 in MAECs. NO production was decreased in aged wild‐type, CerS2 null, and catalase<SUP>−/−</SUP>/GPX1<SUP>−/−</SUP>MAECs. However, K<SUB>Ca</SUB>3.1 activation‐induced, NG‐nitro‐<SMALL>L</SMALL>‐arginine‐, and indomethacin‐resistant EDR was increased without a change in acetylcholine‐induced EDR in aortic rings from aged wild‐type, CerS2 null, and catalase<SUP>−/−</SUP>/GPX1<SUP>−/−</SUP> mice. CerS5 transfection or exogenous application of sphingosine or sphingosine 1‐phosphate induced similar changes in levels of the antioxidant enzymes and upregulated K<SUB>Ca</SUB>3.1. Our findings suggest that, during aging‐related oxidative stress, SOD upregulation and downregulation of catalase and GPX1, which occur upon altering the sphingolipid composition or acyl chain length, generate H<SUB>2</SUB>O<SUB>2</SUB> and thereby upregulate K<SUB>Ca</SUB>3.1 expression and function via a H<SUB>2</SUB>O<SUB>2</SUB>/Fyn‐mediated pathway. Altogether, enhanced K<SUB>Ca</SUB>3.1 activity may compensate for decreased NO signaling during vascular aging.</P>