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Lipid Mediator에 의한 적혈구 Microvesicle 생성에 대한 연구
정승민(Seung-Min Chung),배옥남(Ok-Nam Bae),노지윤(Ji-Yoon Noh),김수진(Su-Jin Kim),임경민(Kyung-Min Lim),정진호(Jin-Ho Chung) 한국독성학회 2006 Toxicological Research Vol.22 No.4
Lipid mediator such as lysophosphatidic acid (LPA) plays an important role in inflammation and wound healing, has been recently reported to induce influx of extracellular calcium into erythrocytes. This elevation in intracellular calcium level may cause destruction of membrane asymmetry and procoagulant microvesicle formation. Thus, we investigated if the lipid mediator could induce microvesicle formation as a result of extracellular calcium influx in human erythrocytes. Treatment with lipid mediator to erythrocytes resulted in microvesicle generation in a concentration-, timedependent manner. Microvesicles formed expressed procoagulant phosphatidylserine (PS) on their surface membrane significantly as well. LPA did not affect the band 3 phosphorylation which is involved in morphological change in erythrocytes. Pretreatment with suramin did not inhibit LPAinduced microvesicle generation, suggesting microvesicle generation was not receptor-dependent pathway. Depletion of intracellular ATP levels in erythrocytes was suggested to be one of the mechanism for these events.
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목초액의 혈소판 응집억제를 통한 혈행개선 작용에 관한 연구
김영대(Young-Dae Kim),배옥남(Ok-Nam Bae),정승민(Seung-Min Chung),정진호(Jin-Ho Chung) 한국독성학회 2004 Toxicological Research Vol.20 No.2
We investigated the effects of plant vinegar on platelets and blood coagulation system. Plant vinegar inhibited in vitro platelet aggregation in a concentration dependent manner, when platelets were activated by thrombin and collagen. In addition, plant vinegar showed inhibitory effects on the serotonin secretion induced by thrombin in a concentration dependent manner. However, treatment<br/> with plant vinegar to platelets did not induce any cytotoxicity, as determined by the release of lactate dehydrogenase. Plant vinegar did not change the coagulation parameters such as activated partial thromboplastin time (aPTT) and prothrombin time (PT) using rat citrated plasma. In vivo study revealed that, treatment with plant vinegar prolonged the bleeding time from mouse tail. All these<br/> results suggest that plant vinegar might improve blood hemostasis mediated via antiplatelet activities.
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목초액의 혈소판 응집억제를 통한 혈행개선 작용에 관한 연구
김영대(Young-Dae Kim),배옥남(Ok-Nam Bae),정승민(Seung-Min Chung),정진호(Jin-Ho Chung) 한국독성학회 2004 Toxicological Research Vol.20 No.1
We investigated the effects of plant vinegar on platelets and blood coagulation system. Plant vinegar inhibited in vitro platelet aggregation in a concentration dependent manner, when platelets were activated by thrombin and collagen. In addition, plant vinegar showed inhibitory effects on the serotonin secretion induced by thrombin in a concentration dependent manner. However, treatment<br/> with plant vinegar to platelets did not induce any cytotoxicity, as determined by the release of lactate dehydrogenase. Plant vinegar did not change the coagulation parameters such as activated partial thromboplastin time (aPTT) and prothrombin time (PT) using rat citrated plasma. In vivo study revealed that, treatment with plant vinegar prolonged the bleeding time from mouse tail. All these<br/> results suggest that plant vinegar might improve blood hemostasis mediated via antiplatelet activities.
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Donghyun Kim(김동현),Ok-Nam Bae(배옥남) 환경독성보건학회 2021 한국독성학회 심포지움 및 학술발표회 Vol.2021 No.5
The role of blood-brain barrier (BBB) dysfunction in various neurological/vascular diseases is well established. BBB is a gatekeeper, which strictly regulates the molecular transportation between systemic circulation and the central nervous system (CNS). Since environmental substances can enter the blood circulation and be exposed to vascular endothelium, it is important to evaluate these substances altering the function of BBB. Isothiazolinone (IT) biocides are potent anti-bacterial substances commonly used as preservatives and disinfectants. In this study, we used three representing IT biocide, benzisothiazolinone (BIT), 4,5-dichloro-2-n-octyl-isothiazolin-3-one (DCOIT), and 2-n-octyl-4-isothiazolin-3-one (OIT) to investigate its effect on the function of in vitro BBB models. We compared the IC50 (50% inhibitory concentration) of three IT biocides on mitochondrial metabolic capacity in bEND.3 cells. And the effects of these substances on oxidative stress and mitochondrial bioenergetics were examined as the molecular mechanism of BBB dysfunction. Of note, augmentation effects of IT biocide on metabolic capacity in brain ECs under hypoxic- or glycative-stress, simulating the ischemic- or diabetic-pathological condition, respectively, were observed. Here, we suggested that the IT biocides induced the BBB dysfunction through the increased oxidative stress and damage on mitochondrial bioenergetics or dynamics and that these substances might increase the hypoxic or glycative stress in the brain endothelium.
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