• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.5
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• pp.635-641
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• 2011

Anti-atherogenic effects in tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated human umbilical vein endothelial cells (HUVEC) are involved with suppressed oxidative stress, cell adhesion molecules, and pro-inflammatory factors. The aim of this study was to determine whether green tea seed coat ethyl acetate fraction (GTSCE) could modulate cell adhesion molecules and inflammatory mediators in HUVEC stimulated with TNF-${\alpha}$. Nitric oxide (NO) production was significantly increased in TNF-${\alpha}$-stimulated HUVEC compared to TNF-${\alpha}$ only treated cells. The NO that is produced by endothelial nitric oxide synthase dilates blood vessels and has protective effects against platelet and leucocyte adhesion. GTSCE at 25, 50, 75, and $100\;{\mu}g$/mL significantly (p<0.05) reduced TNF-${\alpha}$ production. GTSCE significantly (p<0.05) inhibited soluble vascular cell adhesion molecule-1 level, in a dose-dependent manner. Monocyte chemoattractant protein-1 level was also significantly (p<0.05) inhibited by GTSCE treatment at $75\;{\mu}g$/mL compared to the TNF-${\alpha}$-only treated group. Total antioxidant capacity by GTSCE was significantly (p<0.05) enhanced compared to the TNF-${\alpha}$-only treated group. These results suggest that GTSCE can inhibit the production of cell adhesion molecules and inflammatory mediators and could be used as a candidate bioactive material to prevent the development of atherosclerosis.

• Journal of Chest Surgery
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• v.35 no.2
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• pp.87-93
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• 2002

Background: Predicting the important role of intercellular adhesion molecule-1 expression on the acute ischemia-reperfusion injury, we set out to demonstrate it by assessing the degree of expression of ICAM-1 after warm ischemia-reperfusion in canine unilateral lung ischemia model. Material and Method: Left unilateral lung ischemia was induced by clamping the left hilum for 100 minutes in seven adult mongrel dogs. After reperfusion, various hemodynamic pararmeters and blood gases were analyzed for 4 hours, while intermittently clamping the right hilum in order to allow observation of the injured Ieft lung function. The pulmonary venous blood was collected serially to measure TNF- and cICAM-1 level. After 4 hours of reperfusion, the lung tissue was biopsied to assess cICAM-1 expression, and to measure tissue malondialdehyde(MDA) and ATP level. Result: The parameters including arterial oxygen partial pressure, pulmonary vascular resistance and tissue MDA and ATP level suggested severe lung damage. Serum TNF-$\alpha$ level was 8.76$\pm$2.37 ng/ml at 60 minutes after reperfusion and decreased thereafter. The cICAM-1 level showed no change after the reperfusion during the experiment. The tissue cICAM-1 expression was confirmed in 5 dogs. Conclusion: The increase of TNF-$\alpha$ Ievel and expression of tissue ICAM-1 were demonstrated after ischemia reperfusion injury in canine lung model.

• Journal of Korean Medicine Rehabilitation
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• v.33 no.3
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• pp.47-65
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• 2023

Objectives We evaluated the wound healing effects of Dangguijakyak-san (DJ) using C57BL/6 mice that were generated open wound. Methods The study was conducted with seven C57BL/6 mice assigned to each group, divided into the normal group, control group, vitamin E group, DJ low-dose group, DJ high-dose group. We measured total polyphenol, flavonoid contents, the size of the wound, liver function, pro-inflammatory cytokine activity in serum, inflammation-related proteins, adhesion molecules and chemokine proteins, collagen-related proteins in skin tissue and histopathological changes by H&E and Masson's staining. Results DJ treatment significantly reduced the area of the wound compared to the control group. Also, inflammatory cytokines were reduced and the expression of anti-inflammatory-related factors (interleukin-4 [IL-4] and IL-10) was significantly increased in the DJ treatment group. We identified that DJ treatment inhibits both pathways of inflammation, the mitogen-activated protein kinases and nuclear factor-κB pathway. Moreover, the protein expressions of Sirt1 (sirtuin 1), MCP-1 (monocyte chemoattractant protein 1), ICAM-1 (intercellular adhesion molecule 1), and VCAM-1 (vascular cell adhesion molecule 1) were decreased by DJ administration. Also, the expression of α-smooth muscle actin and collagen type I alpha 1, collagen-related proteins, that help skin recovery was significantly increased in the DJ treatment group. Histopathologically, a relatively thin epithelial layer could be observed in the DJ administration group, as well as an increase in fibroblasts and collagen fibers. Conclusions These data suggest that DJ treatment is effective in wound healing, suppressing inflammatory proteins, increasing skin repair factors and improving histopathological changes caused by wounds.

• Journal of Periodontal and Implant Science
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• v.50 no.5
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• pp.291-302
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• 2020

Purpose: The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs). Methods: Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase. Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H₂O₂) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses. Results: Glucose-induced oxidative stress led to increased production of H₂O₂, with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress. Conclusions: This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.

• Korean Journal of Head & Neck Oncology
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• v.18 no.1
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• pp.23-29
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• 2002

Mutation of the P53 tumor suppressor gene playa major role in the development of many carcinomas, namely in the colon, breast and bladder, whereas the role played by such mutations in thyroid carcinogenesis remains controversial. Vascular endothelial growth factor (VEGF) induces proliferation of endothelial cells, stimulates angiogenesis, and increases vascular permeability. Increased VEGF expression has been associated with poor clinical outcomes in many malignancies E-cadherin, a calcium-dependent transmembrane glycoprotein, is an adhesion molecule Expression of p53, VEGF and E-cadherin was assessed immunohistochemically in 19 tall columnar variant of papillary carcinoma, 24 common papillary carcinoma and 7 follicular carcinoma. The aim of this study was to evaluate the expression of P53,VEGF and E-cadherin as a potential maker for the prognosis of thyroid carcinomas. The results are as follows: 1) There were no significance in any clinical parameters examined among tall columnar variant of papillary carcinoma, common papillary carcinoma and follicular carcinoma. 2) The expression of P53 demonstrated low in tall columnar variant of papillary carcinoma, common papillary carcinoma and follicular carcinoma, but a significantly high in regional lymph node metastasis. 3) The expression of VEGF demonstrated a significantly high in regional lymph node metastasis than those without metastasis in papillary thyroid carcinoma. 4) The expression of E-cadherin demonstrated less often among papillary carcinomas with lymph node metastasis than in those without metastasis in papillary thyroid carcinoma. In conclusion, it is suggested that VEGF and E-cadherin will be useful for the diagnosis of thyroid carcinoma and serves as a biological marker for thyroid carcinoma lymph node metastasis.

• Korean Journal of Pharmacognosy
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• v.54 no.1
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• pp.21-26
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• 2023

Cirsium japonicum var. maackii is a traditional Korean wild perennial herb used to treat blood circulation, high blood pressure, inflammation, diabetes, and kidney damage. However, it is not known whether C. japonicum var. maackii directly improves endothelial dysfunction. In this study, the effect of C. japonicum var. maackii (CJE) on tumor necrosis factor (TNF)-α-induced vascular inflammation was investigated in vitro using human umbilical vein endothelial cells (HUVEC). As a result, CJE inhibited the production of VCAM-1, ICAM-1 and ROS increased by TNF-α in HUVECs. In addition, treatment with CJE attenuated IκB phosphorylation and translocation of NF-κB to the nucleus. These results suggest that CJE can suppress TNFα-induced adhesion molecule expression by blocking NF-κB signaling and inhibiting ROS generation. The results of this study show that CJE has the potential to be used to treat and prevent inflammation associated with endothelial cell damage.

• International Journal of Oral Biology
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• v.35 no.1
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• pp.27-33
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• 2010

Periodontal disease is a major oral disorder and comprises a group of infections that lead to inflammation of the gingiva and the destruction of periodontal tissues. $PPAR{\gamma}$ plays an important role in the regulation of several metabolic pathways and has recently been implicated in inflammatory response pathways. However, its effects on periodontal inflammation have yet to be clarified. In our current study, we evaluated the anti-inflammatory effects of $PPAR{\gamma}$ on periodontal disease. Human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) showed high levels of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 (MMP-2), and -9 (MMP-9). Moreover, these cells also showed upregulated activities for extracellular signal regulated kinase (ERK1/2), inducible nitric oxide synthase (iNOS) and cyclooxygnase-2. However, cells treated with Ad/$PPAR{\gamma}$ and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of $PPAR{\gamma}$ appear to be mediated via the suppression of the ERK1/2 pathway and consequent inhibition of NF-kB translocation. Our present findings thus suggest that $PPAR{\gamma}$ indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4369-4376
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• 2015

Background: To investigate in-vitro antagonistic effect of low-dose liquiritigenin on gemcitabine-induced capillary leak syndrome (CLS) in pancreatic adenocarcinoma via inhibiting reactive oxygen species (ROS)-mediated signalling pathways. Materials and Methods: Human pancreatic adenocarcinoma Panc-1 cells and human umbilical vein endothelial cells (HUVECs) were pre-treated using low-dose liquiritigenin for 24 h, then added into gemcitabine and incubated for 48 h. Cell viability, apoptosis rate and ROS levels of Panc-1 cells and HUVECs were respectively detected through methylthiazolyldiphenyl-tetrazoliumbromide (MTT) and flow cytometry. For HUVECs, transendothelial electrical resistance (TEER) and transcellular and paracellular leak were measured using transwell assays, then poly (ADP-ribose) polymerase 1 (PARP-1) and metal matrix proteinase-9 (MMP9) activity were assayed via kits, mRNA expressions of p53 and Rac-1 were determined through quantitative polymerase chain reaction (qPCR); The expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and PARP-1 were measured via western blotting. Results: Low-dose liquiritigenin exerted no effect on gemcitabine-induced changes of cell viability, apoptosis rate and ROS levels in Panc-1 cells, but for HUVECs, liquiritigenin ($3{\mu}M$) could remarkably elevate gemcitabine-induced decrease of cell viability, transepithelial electrical resistance (TEER), pro-MMP9 level and expression of ICAM-1 and VCAM-1 (p<0.01). Meanwhile, it could also significantly decrease gemcitabine-induced increase of transcellular and paracellular leak, ROS level, PARP-1 activity, Act-MMP9 level, mRNA expressions of p53 and Rac-1, expression of PARP-1 and apoptosis rate (p<0.01). Conclusions: Low-dose liquiritigenin exerts an antagonistic effect on gemcitabine-induced leak across HUVECs via inhibiting ROS-mediated signalling pathways, but without affecting gemcitabine-induced Panc-1 cell apoptosis. Therefore, low-dose liquiritigenin might be beneficial to prevent the occurrence of gemcitabine-induced CLS in pancreatic adenocarcinoma.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.396-401
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• 2007

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate metter (PM) effect on intercellular. adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in asthma-induced Balb/c and IL-10 knock out (KO) mouse. Mouse was sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After induction of asthma mouse placed in the inhalation chamber and exposed to DEP and PM (10 $mg/m^3$). The evidences of pulmonary inflammation were assessed by immunohistochemical stain and westen blot against ICAM-1 and VCAM-1 in the lung tissue. In the immunohistochemical stain, positive reactions for ICAM-1 and VCAM-1 were much stronger in asthma-induced groups and asthma-induced group with DEP or PM than control groups. Although mild positive reactions were appeared in asthma-induced IL-10 KO mice groups, positive reactions were very strong in the asthma-induced group with DEP or PM. In Western blot, expression of VCAM-1 was increased in asthma-induced group with DEP or PM than asthma-induced groups. In the IL-10 KO mouse, ICAM-1 and VCAM-1 expression were increased in asthma-induced group with DEP or PM than asthma-induced groups. DEP and PM exposure have additive effects on the aggravation of inflammatory signs in the asthma-induced murine model. These results suggest that inhalation of DEP and PM in asthmatic patients may aggravate clinical symptoms.

• IMMUNE NETWORK
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• v.1 no.1
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• pp.87-94
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• 2001

Background: Cytokine-mediated ex vivo expansion has been proposed as a means of increasing the number of cord blood (CB) hematopoietic stem cells for transplantation. As well as stem cell number, stromal cells are necessary for functional maturation of hematopoiesis. The purpose of this study was to analyze the development of stromal cells during ex vivo expansion of CB $CD34^+$ cells. Methods : $CD34^+$ cells were purified from CB by magnetic bead selection. The levels of of interleukin-3, interleukin-$1{\beta}$, interleukin-6, granulocyte macrophagecolony stimulating factor and tumor necrosis factor-${\alpha}$ were measured in culture supernatants on 0, 1, 2, and 3 weeks, using ELISA techniques. CB $CD34^+$ cells were expanded in Iscoves modified Dulbeccos medium in the presence of several cytokines. The expression of E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, platelet/endothelial cell adhesion molecule-1, von Willebrand factor, vimentin, and CD14 in newly developed stromal cells was examined by immunocytochemical method. Relevant extracellular matrix (ECM) proteins and proper cytokines were also assayed for the most suitable condition for expansion of stromal cells. Results: Several cytokines were found to have been produced by CB $CD34^+$ cells as well as bone marrow-derived $CD34^+$ cells. During ex vivo expansion of CB $CD34^+$ cells, stromal cells appeared in the culture by day 4 and expanded over the following 7-10 days before being confluent by day 2 1. These cells expressed surface markers characteristic of cells of endothelial lineage. Furthermore, these stroaml cells also expanded effectively when treated with thrombopoietin+flt-3 ligand+stem cell factor+leukemia inhibitory factor or 0.1% poly-L-lysine-coated wells. Conclusion: Stromal cells were developed during ex vivo expansion of CB $CD34^+$ cells and that this development could be enhanced further by treating the stromal cells with cytokines or ECM.