• Bulletin of the Korean Chemical Society
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• 제34권2호
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• pp.406-410
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• 2013

Tetrahyropapaveroline (THP) is compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegenerative disorder, such as Parkinson's disease (PD). The aim of this study was to evaluate the potential of THP to cause oxidative damage on the structure of cytochrome c (cyt c). Our data showed that THP led to protein aggregation and the formation of carbonyl compound in protein aggregates. THP also induced the release of iron from cyt c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the THP-mediated cyt c modification and carbonyl compound formation. The results of this study show that ROS may play a critical role in THP-induced cyt c modification and iron releasing of cyt c. When cyt c that has been exposed to THP was subsequently analyzed by amino acid analysis, lysine, histidine and methionine residues were particularly sensitive. It is suggested that oxidative damage of cyt c by THP might induce the increase of iron content in cells and subsequently led to the deleterious condition. This mechanism is associated with the deterioration of organs under neurodegenerative disorder such as PD.

• Journal of Ginseng Research
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• 제18권1호
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• pp.44-48
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• 1994

In adrenaline-stimulated human platelets, panaxadiol (PD) and panaxatriol (PT) from Panax ginseng C.A. Meyer did not inhibit the $Ca^{2+}$-innux, but inhibited the formation of thromboxane $A_2$ and the platelet aggregations. It seems that PD and PT block a pathyway interconvefing arachidonic acids (20:4) to thromboxane $A_2$ (TX $A_2$), because the amount of $Ca^{2+}$ which phospholipase C or phospholipase $A_2$ requires to liberate 20 : 4 from membrane phospholipids was increased by PD and PT. These results mean that PH and PT have an antiplatelet effect by Inhibiting the formation of TX $A_2$.

• 생약학회지
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• 제51권4호
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• pp.231-237
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• 2020

Euchrestaflavanone B (EFB) is a flavonoid that can be found in root bark, particularly in Cudrania tricuspidata (C. tricuspidata). The extract of C. tricuspidata is widespread throughout Asia and used in traditional medicine. In a previous study, we found anti-platelet effects of substances isolated from C. tricuspidata on collagen-induced human platelets. However, the C. tricuspidata still contains numerous substances, thus, we have searched new candidate, EFB isolated from C. tricuspidata for anti-platelet effect. Our results showed that EFA inhibited collagen-induced platelet aggregation and glycoprotein IIb/IIIa (αIIb/β3)-mediated signaling events, including platelet adhesion, granule secretion, thromboxane A2 production and clot retraction. These results suggest that EFA has inhibitory effects on human platelet activities and thrombus formation and has potential value as a natural substance for preventing platelet-induced thrombosis.

• 한국식품과학회지
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• 제29권4호
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• pp.817-822
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• 1997

구름버섯 자실체에서 분리된 항응고성 다당류의 혈액응고 저해기작을 검토하였다. 항응고성 다당(CV-40-Va-1)은 vWF의 활성을 감소시킴으로써 혈소판응집을 억제시키는 것으로 나타났으며, 혈액응고인자중 thrombin뿐만이 아니라 내인성경로의 factor VII, IX, XI, XII의 활성 또한 억제 하였다. 그러나 CV-40-Va-1의 항응고 활성은 thromin에 직접 작용하는 것이 아니라 antithrombin III 의존적 활성을 보였다. Sulfation에 의하여 CV-40-Va-1의 항응고활성의 증가와 다당의 desulfation시 상반된 결과에서 CV-40-Va-1의 황산기가 항응고활성의 중요한 인자임을 알 수 있었다. CV-40-Va-1을 TFA로 부분가수분해하여 얻은 획분들(Fr.I, Fr.II)에서는 항응고 활성이 감소하였으나 분자량 1,000정도로 추정되는 획분(Fr.II)은 오히려 혈소판응집을 강력하게 억제하였다.

• Journal of Microbiology and Biotechnology
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• 제29권8호
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• pp.1177-1183
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• 2019

Grapefruit seed extract (GSE) is a safe and effective preservative that is used widely in the food industry. However, there are few studies addressing the anti-biofilm effect of GSE. In this study, the anti-biofilm effect of GSE was investigated against biofilm-forming strains of Staphylococcus aureus and Escherichia coli. The GSE minimum inhibitory concentration (MIC) for S. aureus and E. coli were $25{\mu}g/ml$ and $250{\mu}g/ml$, respectively. To investigate biofilm inhibition and degradation effect, crystal violet assay and stainless steel were used. Biofilm formation rates of four strains (S. aureus 7, S. aureus 8, E. coli ATCC 25922, and E. coli O157:H4 FRIK 125) were 55.8%, 70.2%, 55.4%, and 20.6% at $1/2{\times}MIC$ of GSE, respectively. The degradation effect of GSE on biofilms attached to stainless steel coupons was observed (${\geq}1$ log CFU/coupon) after exposure to concentrations above the MIC for all strains and $1/2{\times}MIC$ for S. aureus 7. In addition, the specific mechanisms of this anti-biofilm effect were investigated by evaluating hydrophobicity, auto-aggregation, exopolysaccharide (EPS) production rate, and motility. Significant changes in EPS production rate and motility were observed in both S. aureus and E. coli in the presence of GSE, while changes in hydrophobicity were observed only in E. coli. No relationship was seen between auto-aggregation and biofilm formation. Therefore, our results suggest that GSE might be used as an anti-biofilm agent that is effective against S. aureus and E. coli.

• BMB Reports
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• 제44권2호
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• pp.140-145
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• 2011

Impaired responsiveness of platelets to epinephrine (epi) and other catecholamines (CA) has been reported in approximately 20% of the healthy Korean and Japanese populations. In the present study, platelet aggregation induced by epi was potentiated by RO 31-8220 (RO) or G$\ddot{o}$ 6983 (G$\ddot{o}$). Phosphorylated Akt (p-Akt) was very low in epi-stimulated PRP from CA-hypo- responders (CA-HY), whereas it was detected in those from CA-good responders (CA-GR). RO and G$\ddot{o}$ increased p-Akt, one of the major downstream effectors of phosphoinositol-3 kinase (PI3K), in epi-stimulated PRP from both groups. Wortmannin, a PI3K inhibitor, attenuated the RO or G$\ddot{o}$-induced potentiation of p-Akt in epi-stimulated PRP, suggesting positive effects for RO and G$\ddot{o}$ on PI3K. $TXA_2$ formation was increased by the addition of either RO or G$\ddot{o}$ in epi-stimulated platelets. The present data also suggest that impaired Akt phosphorylation may be responsible for epinephrine hypo-responsiveness of platelets.

• Korea-Australia Rheology Journal
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• 제20권3호
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• pp.109-116
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• 2008

The effect of intermolecular aggregation induced by hydrophobic and electrostatic interactions on shear and elongational flow properties of aqueous acrylic thickener solutions is discussed. Complex shear modulus is determined at frequencies up to $10^4$ rad/s employing oscillatory squeeze flow. Extensional flow behavior is characterized using Capillary Break-up Extensional Rheometry. Aqueous solutions of poly(acrylic acid)(PAA)/poly(vinylpyrrolidone-co-vinylimidazole) (PVP-VI) mixtures exhibit unusual rheological properties described here for the first time. Zero-shear viscosity of the mixtures increases with decreasing pH and can exceed that of the pure polymers in solution by more than two orders of magnitude. This is attributed to the formation of complexes induced by electrostatic interactions in the pH range, where both polymers are oppositely charged. PAA/PVP-VI mixtures are compared to the commercial thickener Sterocoll FD (BASF SE), which is a statistical co-polymer including (meth) acrylic acid and ethylacrylate (EA) forming aggregates in solution due to "sticky" contacts among hydrophobic EA-sequences. PAA/PVP-VI complexes are less compact and more deformable than the hydrophobic Sterocoll FD aggregates. Solutions of PAA/PVP-VI exhibit a higher zero-shear viscosity even at lower molecular weight of the aggregates, but are strongly shear-thinning in contrast to the weakly shear-thinning solutions of Sterocoll FD. The higher ratio of characteristic relaxation times in shear and elongation determined for PAA/PVP-VI compared to Sterocoll FD solutions reflects, that the charge-induced complexes provide a much stronger resistance to extensional flow than the aggregates formed by hydrophobic interactions. This is most likely due to a break-up of the latter in extensional flow, while there is no evidence for a break-up of complexes for PAA/PVP-VI mixtures. These flexible aggregates are more suitable for the stabilization of thin filaments in extensional flows.

• 대한한의학회지
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• 제29권5호
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• pp.52-66
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• 2008

Objectives :Ginkgo-Chunghyul-dan (GCHD) is newly developed herbal medicine to prevent and treat stroke. In this study, we investigated whether the GCHD had antioxidant activity and anti-platelet aggregation effect in vitro and hypolipidemic activities in vivo. Methods :Anti-oxidant activity of GCHD was measured using the Blois method, anti-platelet effect of GCHD was assessed by the Born method, and hypolipidemic activities of GCHD were evaluated in corn oil- or Triton WR-1339-induced and cholesterol-fed rats. Results :GCHD showed anti-oxidant activity in the study inhibiting the formation of 1-diphenyl-2-picrylhydrazyl radicals and xanthine oxidase activity. GCHD had anti-platelet aggregation activity. GCHD significantly lowered total cholesterol (TC), triglyceride (TG), and low density lipoprotein cholesterol (LDL-C) in high cholesterol diet and Triton WR-1339 induced model TG in corn oil-induced model. GCHD had no acute toxicity at a single dosage. Conclusion : These results suggest that GCHD has the potential to treat hyperlipidemia and stroke.

• 약학회지
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• 제43권6호
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• pp.809-817
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• 1999

The effect of 2-(4-cyanophenyl)amino-1,4-naphthalenedione-3-pyridinium perchlorate (PQ5) on pla-telet aggregation and its action mechanisms were investigated with rat platelet. PQ5 inhibited the platelet aggregation induced by collagen ($6{\;}{\mu\textrm{g}}/ml$), thrombin (0.4 U/ml) and A23187 ($3{\mu}M$) in concentration-dependent manner with $IC_{50}$ values of 5.50, 25.89 and $37.12{\;}{\mu}M$, respectively. PQ5 also significantly reduced the thromboxane $A_2$ (TXA2) formation in a concentration dependent manner. The collagen-induced arachidonic acid (AA) release in [-3H]-AA incorporated platelet, an indication of the phospholipase $A_2$ activity, was decreased by PQ5 pretreatment PQ5 significantly inhibited the activity of thormboxane synthase only at high concentration ($100{\mu}M$), but did not affect the cyclooxygenase activity at all. Collagen-induced ATP release was significantly reduced by PQ5. Calcium-induced platelet aggregation experiment suggests that the elevation of intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) by collagen stimulation is decreased by the pretreatment of PQ5, which is due to the inhibition of calcium release from intracellular store and influx from outside of the cell. PQ5 did not showed the effect of anticoagulation as prothrombin time (PT) or activated partial thromboplastin time (APTT). Form these results, it is suggested that PQ5 exerts its antiplatelet activity through the inhibition of the intracellular $Ca^{2+}$ mobilization and the decrease of the $TXA_2$ synthesis.

• Journal of Ginseng Research
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• 제45권4호
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• pp.490-497
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• 2021

Background and objective: Synthetic ginsenoside compounds G-Rp (1,3, and 4) and natural ginsenosides in Panax ginseng 20(S)-Rg3, Rg6, F4 and Ro have inhibitory actions on human platelets. However, the inhibitory mechanism of ginsenoside Rk1 (G-Rk1) is still unclear thus, we initiated investigation of the anti-platelet mechanism by G-Rk1 from Panax ginseng. Methodology: Our study focused to investigate the action of G-Rk1 on agonist-stimulated human platelet aggregation, inhibition of platelet signaling molecules such as fibrinogen binding with integrin α_IIbβ₃ using flow cytometry, intracellular calcium mobilization, fibronectin adhesion, dense granule secretion, and thromboxane B2 secretion. Thrombin-induced clot retraction was also observed in human platelets. Key Results: Collagen, thrombin, and U46619-stimulated human platelet aggregation were dose-dependently inhibited by G-Rk1, while it demonstrated a more effective suppression on collagen-stimulated platelet aggregation using human platelets. Moreover, G-Rk1 suppressed collagen-induced elevation of Ca²⁺ release from endoplasmic reticulum, granule release, and α_IIbβ₃ activity without any cytotoxicity. Conclusions and implications: These results indicate that G-Rk1 possess strong anti-platelet effect, proposing a new drug candidate for treatment and prevention of platelet-mediated thrombosis in cardiovascular disease.