• 대한수의학회지
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• 제36권4호
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• pp.873-886
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• 1996

For better understanding the interrelationship of hemorrhage and aggregation mechanism, cyclopiazonic acid(CPA) known as promoting the aggregation of platelet, aflatoxin $B_1(AFB_1)$ inhibiting platelet aggregation were used as toxic mycotoxins in these studies. In order to investigate the potential role of prostaglandin metabolism on the platelet aggregation, a variety of prostaglandin metabolites such as $PGF_{2{\alpha}}$, $PGE_2$ and $TXB_2$ were measured in homogenized rabbit platelets by TLC and LSC. And the role of $Ca^{{+}{+}}$ on the platelet aggregation was investigated by flow cytometer. Finally, the morphological effects of mycotoxins on platelet were determined by transmission electron microscope. The results and conclusions obtained from these studies are: 1) CPA induced no changes but $AFB_1$ increased $PGE_2$ and $TXB_2$. 2) CPA promoted ADP, collagen, thrombin, A.A., and PAF-induced $Ca^{{+}{+}}$ release. $AFB_1$, however, decreased $Ca^{{+}{+}}$ level except collagen-induced $Ca^{{+}{+}}$ release. When the calcium blocker, verapamil, was used, CPA decreased thrombin-induced $Ca^{{+}{+}}$ release and increased collagen, ADP, PAF and A.A.-induced $Ca^{{+}{+}}$ release. $AFB_1$ in contrast decreased the all factors induced $Ca^{{+}{+}}$ release. 3) $AFB_1$ did not induce any ultrastructural changes except large vacuole formation in a few platelets. And CPA also did not induce any changes except moderate shape change, indicator of platelet activation. In conclusion, CPA promoted platelet aggregation by the increases of $Ca^{{+}{+}}$ release but had no changes in A.A. metabolites. Antiaggregating effects of $AFB_1$ may be due to decreases of $Ca^{{+}{+}}$ release and increases of $PGE_2$ and $PGF_{2{\alpha}}$ formation. These data provide the basis for the future study of mobilization and function of $Ca^{{+}{+}}$ in platelet aggregation.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 1984년도 학술대회지
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• pp.191-197
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• 1984

인삼의 저혈당성 분획 (DPG-3-2)이 적출한 랑겔한스섬에서 인슐린 분비를 증가시킨다고 일전에 본 저자들이 발표하였다. 근래에 이와 같은 DPG-3-2 분획으로부터 사포닌, 뉴크레오사이드, 뉴크레오타이드, 아미노산, 당 등을 완전히 제거시켜 더욱 정제한 D-O-ANa 성분을 추출하였다. D-O-ANa 유발성 인슐린 분비효과를 DPG 3-2 분획과 그외 잔여성분과 비교 검토하였다. D-O-ANa는 글루코우즈 농도의 고저에 무관하게 인슐린 분비를 가장 강하게 촉진하였다. 특히 D-O-ANa는 제 2 차증 글루코운즈 유발성 인슐린 분비를 촉진하였다. DPG 3-2 분획은 당뇨병 쥐로부터 떼어낸 랑겔한스섬에서 세포외 체액의 칼슘이온이 증가됨에 따라($0.16{\~}6.25$mM) 글루코우즈 유발성 인슐린 분비를 더욱 현저히 증가시켰다. 칼슘이온 흡수와 인슐린분비의 상호관계가 뚜렷이 밝혀졌다. 이 관계는 single sucrose gap 방법에 의해 주의 적출 간 문맥에서 칼슘주파수가 증가되는 실험을 통해 증명되었다.

• BMB Reports
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• 제28권4호
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• pp.301-305
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• 1995

Considering the stimulatory effects of ginsenosides from Panax ginseng C. A. Meyer on the release of nitric oxide from bovine aortic endothelial cells in vitro and vasodilatation of rabbit pulmonary artery in vivo, the present study is designed to investigate the mechanism of nitric oxide release by ginsenosides in calf pulmonary artery endothelial cells, Nitric oxide release was determined in endothelial cells treated with ginsenosides and compared with those of the receptor-dependent agonists, bradykinin and ADP and the receptor-independent calcium ionophore $A_{23187}$. The results showed that total saponin and ginsenoside $Rg_1$, not $Rb_1$, stimulated nitric oxide release measured as conversion to L-citrulline. The nitric oxide releasing properties of total saponin and ginsenoside $Rg_1$ were different; total saponin stimulated only conversion to L-citrulline, like $A_{23187}$, while ginsenoside $Rg_1$ stimulated both L-arginine transport and conversion to L-citrulline, as bradykinin or ADP did.

• Archives of Pharmacal Research
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• 제18권5호
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• pp.295-300
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• 1995

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.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.247.1-247.1
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• 2003

Iron deficiency is the most common nutritional problem worldwide. Oral iron supplementation programs have failed because of noncompliance and gastrointestinal toxicity. The purpose of this study was to explore the possibility of alginate gel bead as an oral controlled release system of iron supplements and increase the stability of iron succinyl casein (ISC). Alginate beads containing ISC were prepared by the gelation of sodium alginate with calcium cations. The release profiles of ISC were investigated according to the concentration of polymer, the drug/sodium alginate ratio, the concentration and type of cation, curing time and pH of calcium chloride solution. (omitted)

• International Journal of Oral Biology
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• 제40권4호
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• pp.211-216
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• 2015

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium ($BK_{ca}$) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of $Ca^{2+}$ that induces $Ca^{2+}$-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective $BK_{Ca}$ channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove $Ca^{2+}$ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through $BK_{ca}$ channels, which are activated by intracellular $Ca^{2+}$ increase via activation of RyR of $Ca^{2+}$ stores.

• Advances in Traditional Medicine
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• 제8권2호
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• pp.178-186
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• 2008

In this study, ionotropic gelation method was used for the preparation of ibuprofen-loaded calcium alginate (CALG) and ethylenediamine (EDA) treated calcium alginate (EDA-CALG) microspheres. The effect of EDA-treatment on drug entrapment efficiency, particle size, morphology, swelling behavior and in vitro release characteristics of the microspheres was investigated by varying its concentration from 0.5 to 2% (v/v). The reduction in drug entrapment efficiency by a maximum of 44.60% was noted for EDA-CALG microspheres compared to untreated CALG microspheres. The particle size and swelling index of EDA-CALG microspheres were reduced with increasing EDA concentration. All the microspheres were observed to retain their spherical shapes with rough surfaces. EDA-CALG microspheres prepared using 1% and 2% v/v EDA, released almost all of its content within 7 h in pH 6.8 phosphate buffer, however, CALG microspheres were found to release the same within 3 h. The intensity of melting endothermic peak of ibuprofen reduced significantly at lower drug load as experienced from DSC thermograms. The FT-IR spectrum of pure ibuprofen, ibuprofen-loaded CALG and EDA-CALG microspheres showed the characteristic band of C = O stretching vibration of ibuprofen. Hence, this study revealed that EDA can be employed for the preparation of ibuprofen-loaded CALG microspheres to retard the drug release to some extent.

• Journal of Pharmaceutical Investigation
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• 제41권2호
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• pp.111-115
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• 2011

pH-sensitive cross-linked polymeric micelles were synthesized by using block ionomer complexes of poly(ethylene oxide)-b-poly(methacrylic acid) (PEO-b-PMA) with calcium ions as micellar templates. An anticancer drug, doxorubicin (DOX) was conjugated on the cross-linked ionic cores of micelles via acid-labile hydrozone bonds. The resulting DOX-conjugated, pH-sensitive micelles are stable at physiological conditions, whereas the release of DOX was significantly increased at the acidic pH. Such micelles were internalized to lysosomes, and acidic pH in lysosomes triggers the release of DOX upon internalization in MCF-7 breast cancer cells. The released DOX entered the cell nucleus and eventually killed cancer cells. Therefore, these data demonstrate that the pH-sensitive micelles could be a promising nanocarrier for delivery of anticancer drug, DOX.

• Preventive Nutrition and Food Science
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• 제21권4호
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• pp.323-329
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• 2016

Achyranthes japonica Nakai (AJN) water extract has a variety of physiological properties, including anti-diabetic, anti-cancer, anti-inflammatory, anti-microbial, and anti-oxidative activities. In the present study, the inhibitory effects of AJN extract were investigated in high affinity immunoglobulin E receptor ($Fc{\varepsilon}RI$)-mediated KU812F cells activation. AJN extract showed suppressive effects on histamine release and intracellular calcium [$Ca^{2+}$]i elevation from anti$Fc{\varepsilon}RI$ antibody (CRA-1)-stimulated cells in a dose-dependent manner. Flow cytometric analysis showed that AJN extract treatment caused a dose-dependent decrease in the cell surface $Fc{\varepsilon}RI$ expression and the binding between the cell surface $Fc{\varepsilon}RI$ and the IgE antibody. Moreover, reverse transcription-polymerase chain reaction analysis showed that levels of the mRNA for the $Fc{\varepsilon}RI$ ${\alpha}$ chain was decreased by treatment with AJN extract. These results indicate that AJN extract may exert anti-allergic effects via the inhibition of calcium influx and histamine release, which occurs as a result from the downregulation of the binding of IgE antibody to cell surface $Fc{\varepsilon}RI$. This mechanism may occur through $Fc{\varepsilon}RI$ expression inhibition.

• Restorative Dentistry and Endodontics
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• 제44권3호
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• pp.24.1-24.1
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• 2019