• Korean Journal of Pharmacognosy
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• v.52 no.1
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• pp.26-33
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• 2021

During blood vessel damage, an essential step in the hemostatic process is platelet activation. However, it is important to properly control platelet activation, as various cardiovascular diseases, such as stroke, atherosclerosis, and myocardial infarction, are also caused by excessive platelet activation. Found primarily in the roots of plants of the genus Artemisia or Scopolia, isoscopoletin has been studied to demonstrate its potential pharmacological effects against Alzheimer's disease and anticancer, but the mechanisms and roles involved in thrombus formation and platelet aggregation are insufficient. This study investigated the effect of isoscopoletin on U46619-induced human platelet activation. As a result, isoscopoletin significantly increased the levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) dose-dependently. In addition, isoscopoletin significantly phosphorylated inositol 1, 4, 5-triphosphate receptor (IP3R) and vasodilator-stimulated phosphprotein (VASP), which are known substrates for cAMP-dependent kinases and cGMP-dependent kinases. Phosphorylated IP3R by isoscopoletin inhibited Ca2+ mobilization from the dense tubular system Ca2+ channels to cytosol, and phosphorylated VASP was involved in the inhibition of fibrinogen binding through αIIb/β3 inactivation in the platelet membrane. Isoscopoletin finally reduced thrombin-induced fibrin clotting production. Therefore, this study suggests that isoscopoletin has a potent antiplatelet effect and may be helpful for platelet-related thrombotic diseases.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.108.2-108.2
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• 2003

Kaempferol, a flavonol compound, has been reported as the anti-oxidant and anti-angiogenic agent and it has been found to inhibit cell growth in vitro. Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays an important role in development of atherosclerosis. In this study, we examined the anti-proliferative effect and its mechanism on rat aortic VSMCs treated by kaempferol. kaempferol significantly inhibited the platelet-derived growth factor (PDGF)-BB-induced proliferation of rat aortic VSMCs in concentration-dependent manner by cell count and ［$^3$H］-thymidine incorporation assay. (omitted)

• Nutrition Research and Practice
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• v.8 no.5
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• pp.521-525
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• 2014

BACKGROUND/OBJECTIVES: Artemisinin (AT), an active compound in Arternisia annua, is well known as an anti-malaria drug. It is also known to have several effects including anti-oxidant, anti-inflammation, and anti-cancer activities. To date, the effect of AT on vascular disorders has not been studied. In this study, we investigated the effects of AT on the migration and proliferation of vascular smooth muscle cells (VSMC) stimulated by platelet-derived growth factor BB (PDGF-BB). MATERIALS/METHODS: Aortic smooth muscle cells were isolated from Sprague-Dawley rats. PDGF-BB stimulated VSMC migration was measured by the scratch wound healing assay and the Boyden chamber assay. Cell viability was determined by using an EZ-Cytox Cell Viability Assay Kit. The production of reactive oxygen species (ROS) in PDGF-BB stimulated VSMC was measured through $H_2DCF$-DA staining. We also determined the expression levels of signal proteins relevant to ROS, including measures of extracellular signal-regulated kinase (ERK) 1/2 measured by western blot analysis and matrix metalloproteinase (MMP) 9 measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: AT ($10{\mu}M$ and $30{\mu}M$) significantly reduced the proliferation and migration of PDGF-BB stimulated VSMC in a dose-dependent manner. The production of ROS, normally induced by PDGF-BB, is reduced by treatment with AT at both concentrations. PDGF-BB stimulated VSMC treated with AT ($10{\mu}M$ and $30{\mu}M$) have reduced phosphorylation of ERK1/2 and inhibited MMP9 expression compared to untreated PDGF-BB stimulated VSMC. CONCLUSIONS: We suggest, based on these results, that AT may exert an anti-atherosclerotic effect on PDGF-BB stimulated VSMCs by inhibiting their proliferation and migration through down-regulation of ERK1/2 and MMP9 phosphorylation.

• The Journal of Korean Obstetrics and Gynecology
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• v.21 no.2
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• pp.125-151
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• 2008

Purpose: In this study, we investigated the anti-thrombotic efficacy of "Eungapbang-gagam(EGB)" currently used in clinical treatment of PID Methods: We studied inhibitory effect of platelet cohesion, suppressive effect of GPIIb/IIIa activity, inhibitory effect of $TXB_2$ and $PGE_2$ biosynthesis, and oxidative damage suppression effects of "EGB" in vitro. Also, suppression of pulmonary embolism and changes of related factors in dextran coagulation condition model were studied in vivo. Results: In this study, EGB extract showed dose-dependent inhibitory effect on platelet coagulation induced by ADP, epinephrine, collagen, arachidonic acid. Also it showed dose-dependent inhibition effect on GPIIb/IIIa activities compared to the control group. EGB extract significantly suppressed the decrease of speed of bloodstream caused by blood coagulation in dextran coagulation condition model and increased the number of platelets and amount of fibrinogen, and decreased the APTT in dextran coagulation condition model compared to the control group. EGB extract showed dose-dependent decrease of oxidative damages caused by DPPH and superoxide anion radicals, whereas dose-dependent increase of superoxide dismutase like activity was observed compared to the control group. Conclusion: We confirmed the anti-thrombosis and anti-oxidative efficacy of "Eungapbang-gagam". Various clinical applications of "Eungapbang-gagam" as well as use of data for the construction of EBM is anticipated.

• The Korean Journal of Blood Transfusion
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• v.29 no.3
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• pp.282-290
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• 2018

Background: Anti-E or paired anti-E/-c antibodies can develop in patients with the Rh CDe phenotype. This study examined the differences in transfusion in patients with the CDe phenotype according to formation of anti-E or anti-E/-c antibodies. Methods: Retrospective reviews were carried out on the results of antibody identification tests performed in 2014. The Rh phenotype and antibody specificity were investigated. The transfusion and medical records of patients with the CDe phenotype were examined. Results: In total, 76 patients were included in the review. Of these 76 patients, 38 (50.0%) were of the CDe phenotype. Anti-E antibodies were the most frequent (60.5%), followed by anti-E/-c antibodies (23.7%). The total transfusion units and platelet transfusion units were significantly higher in patients with anti-E/-c antibodies (P=0.028 and P=0.01, respectively). The distribution of categorized diseases was similar in the patients with the anti-E and anti-E/-c antibodies. A frequency of transfusion episodes greater than or equal to four was higher in patients with hepatobiliary diseases (85.7%). Conclusion: In CDe phenotype patients, platelet transfusion was significantly higher in the anti-E/-c positive group than the anti-E positive group, indicating that platelets play a role in red blood cell alloimmunization. Because E is the most immunogenic antigen in Korea, it is important to define the disease group, in which patients with CDe phenotype require a transfusion of E and c-negative blood.

• Journal of Ginseng Research
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• v.44 no.1
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• pp.24-32
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• 2020

Cardiovascular diseases prevail among modern societies and underdeveloped countries, and a high mortality rate has also been reported by the World Health Organization affecting millions of people worldwide. Hyperactive platelets are the major culprits in thrombotic disorders. A group of drugs is available to deal with such platelet-related disorders; however, sometimes, side effects and complications caused by these drugs outweigh their benefits. Ginseng and its nutraceuticals have been reported to reduce the impact of thrombotic conditions and improve cardiovascular health by antiplatelet mechanisms. This review provides (1) a comprehensive insight into the available pharmacological options from ginseng and ginsenosides (saponin and nonsaponin fractions) for platelet-originated cardiovascular disorders; (2) a discussion on the impact of specific functional groups on the modulation of platelet functions and how structural modifications among ginsenosides affect platelet activation, which may further provide a basis for drug design, optimization, and the development of ginsenoside scaffolds as pharmacological antiplatelet agents; (3) an insight into the synergistic effects of ginsenosides on platelet functions; and (4) a perspective on future research and the development of ginseng and ginsenosides as super nutraceuticals.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.223-230
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• 2017

Platelets play an essential role in hemostasis through aggregation and adhesion to vascular injury sites but their unnecessary activation can often lead to thrombotic diseases. Upon exposure to physical or biochemical stimuli, remarkable platelet shape changes precede aggregation or adhesion. Platelets shape changes facilitate the formation and adhesion of platelet aggregates, but are readily reversible in contrast to the irrevocable characteristics of aggregation and adhesion. In this dynamic phenomenon, complex molecular signaling pathways and a host of diverse cytoskeleton proteins are involved. Platelet shape change is easily primed by diverse pro-thrombotic xenobiotics and stimuli, and its inhibition can modulate thrombosis, which can ultimately contribute to the development or prevention of thrombotic diseases. In this review, we discussed the current knowledge on the mechanisms of platelet shape change and also pathological implications and therapeutic opportunities for regulating the related cytoskeleton dynamics.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.49 no.spc1
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• pp.195-202
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• 2004

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1213-1217
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• 2004

Many ischemic disease patients have been taking herbal medicine and there are some papers that prescription of herbal medicine to ischemic disease patients are useful. Mechanism of herbal medicines on ischmeic disease have been investigated in many ways, but anticougulation or anti platelet effect of herbal medicines is not known obviously. And recently patients receiving anticougulation therapy are discouraged from taking herbal medicines. In this study, we investigate PT, INR, platelet of patients receiving herbal medicine therapy to study whether herbal medicines effect coagulation system of ischemic patients. In PT, INR, platelet values obtained from the patients, before and after administering herbal medicine, there were no significant changes.

• Preventive Nutrition and Food Science
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• v.18 no.3
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• pp.181-187
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• 2013

Artemisia princeps Pampanini (AP) has been used as a traditional medicine in Korea, China and Japan and reported to exhibit various beneficial biological effects including anti-inflammatory, antioxidant, anti-atherogenic and lipid lowering activities; however, its antiplatelet and anticoagulant properties have not been studied. In the present study, we evaluated the effects of an ethanol extract of Artemisia princeps Pampanini (EAP) and its major flavonoids, eupatilin and jaceosidin, on platelet aggregation and coagulation. To determine the antiplatelet activity, arachidonic acid (AA)-, collagen- and ADP (adenosine diphosphate)-induced platelet aggregation were examined along with serotonin and thromboxane A2 ($TXA_2$) generation in vitro. The anticoagulant activity was determined by monitoring the activated partial thromboplastin time (aPTT) and prothrombin time (PT) in vitro. The data showed that EAP and its major flavonoids, eupatilin and jaceosidin, significantly reduced AA-induced platelet aggregation and the generation of serotonin and $TXA_2$, although no significant change in platelet aggregation induced by collagen and ADP was observed. Moreover, EAP significantly prolonged the PT and aPTT. The PT and/or aPTT were significantly increased in the presence of eupatilin and jaceosidin. Thus, these results suggest that EAP may have the potential to prevent or improve thrombosis by inhibiting platelet activation and blood coagulation.