• 미생물학회지
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• 제51권2호
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• pp.156-168
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• 2015

Lactobacillus acidophilus BK13과 Lactobacillus paracasei BK57 균주로부터 얻은 세포, 배양상등액 및 박테리오신 용액의 anti-Helicobacter pylori 활성과 위장상피세포에 대한 세포독성을 평가하였다. 실험균주를 MRS 배지 상에서 30시간 배양한 결과, L. acidophilus BK57 ($126.8{\pm}7.9mM$) 보다 L. paracasei BK57 ($155.9{\pm}7.9mM$)가 더 많은 양의 유산을 생산하였다. 또한, BK13 균주의 최대 박테리오신 활성(128 AU/ml)은 $37^{\circ}C$에서 30시간 배양 후 관찰되었으나, 이는 BK57의 활성(256 AU/ml) 보다는 낮았다. BK13 및 BK57 균주의 살아있는 세포를 H. pylori와 혼합 배양한 결과, 유산균의 초기균수에 의존하여 H. pylori의 저해효과가 나타났다. 게다가 BK13과 BK57로부터 얻은 배양상등액과 박테리오신은 H. pylori의 성장을 억제할 뿐만 아니라 위장상피세포에 대한 부착력과 urease 활성도 저해하였다. 한편, 이러한 균주들이 생산한 유산은 위암세포에 대한 세포독성 효과가 대조구보다 유의한 수준으로 높게 나타났다. 따라서 BK13과 BK57 균주의 항균물질은 위장질환의 원인균인 H. pylori를 저해시키는데 효과적이므로 이들 유산균은 H. pylori 감염으로부터 위장을 보호하는데 유용할 것으로 사료된다.

• The Korean Journal of Physiology and Pharmacology
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• 제19권3호
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• pp.229-234
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• 2015

Nafamostat mesilate (NM) is a serine protease inhibitor with anticoagulant and anti-inflammatory effects. NM has been used in Asia for anticoagulation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation. Oxidative stress is an independent risk factor for atherosclerotic vascular disease and is associated with vascular endothelial function. We investigated whether NM could inhibit endothelial dysfunction induced by tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$ ). Human umbilical vein endothelial cells (HUVECs) were treated with TNF-${\alpha}$ for 24 h. The effects of NM on monocyte adhesion, vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression, p38 mitogenactivated protein kinase (MAPK) activation, and intracellular superoxide production were then examined. NM ($0.01{\sim}100{\mu}g/mL$) did not affect HUVEC viability; however, it inhibited the increases in reactive oxygen species (ROS) production and p66shc expression elicited by TNF-${\alpha}$ (3 ng/mL), and it dose dependently prevented the TNF-${\alpha}$ -induced upregulation of endothelial VCAM-1 and ICAM-1. In addition, it mitigated TNF-${\alpha}$ -induced p38 MAPK phosphorylation and the adhesion of U937 monocytes. These data suggest that NM mitigates TNF-${\alpha}$ -induced monocyte adhesion and the expression of endothelial cell adhesion molecules, and that the anti-adhesive effect of NM is mediated through the inhibition of p66shc, ROS production, and p38 MAPK activation.

• Biomolecules & Therapeutics
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• 제12권4호
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• pp.221-227
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• 2004

Nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the highly selective cyclooxygenase (COX)-2 inhibitors have been shown to decrease the growth of tumor, in part, by inhibition of neovascularization. Recently, besides mature endothelial cells, endothelial progenitor cells (EPCs) have been shown to contribute neovascularization in angiogenic tissues. In this study, we addressed a question whether nimesulide, a selective COX-2 inhibitor, could affect differentiation of EPCs into adhesive endothelial cells in vitro. Total mononuclear cells were isolated from cord blood by Ficoll density gradient centrifugation, and then the cells were incubated with nimesulide or vehicle control for 7 days. The number of adherent and spindle-shaped cells decreased by nimesulide treatment in a concentration-dependent fashion at a concentration range of 5 - 200 ${\mu}M$. Moreover, the adherent cells double positive for DiI-ac-LDL uptake and lectin binding significantly decreased upon nimesulide treatment. There was no change of expression of CD31 between treatment and control groups, whereas slight reduction was detected upon treatment in expression of VE-cadherin, ICAM-1, vWF, ${\alpha}v$, and ${\alpha}5$. Nimesulide also reduced cell viability during first 3 days' culture and induced apoptosis in adherent EPCs, resulting in increased annexin-V-positive and propidium iodide-negative cells. Taken together, these results suggest that nimesulide could be applied for the inhibition of new vessel formation, in part, by inhibiting differentiation and survival of EPCs.