• IMMUNE NETWORK
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• v.23 no.5
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• pp.42.1-42.21
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• 2023

When the lungs are infected with bacteria, alveolar macrophages (AMs) are recruited to the site and play a crucial role in protecting the host by reducing excessive lung inflammation. However, the regulatory mechanisms that trigger the recruitment of AMs to lung alveoli during an infection are still not fully understood. In this study, we identified a critical role for NADPH oxidase 4 (NOX4) in the recruitment of AMs during Staphylococcus aureus lung infection. We found that NOX4 knockout (KO) mice showed decreased recruitment of AMs and increased lung neutrophils and injury in response to S. aureus infection compared to wildtype (WT) mice. Interestingly, the burden of S. aureus in the lungs was not different between NOX4 KO and WT mice. Furthermore, we observed that depletion of AMs in WT mice during S. aureus infection increased the number of neutrophils and lung injury to a similar level as that observed in NOX4 KO mice. Additionally, we found that expression of intercellular adhesion molecule-1 (ICAM1) in NOX4 KO mice-derived lung endothelial cells was lower than that in WT mice-derived endothelial cells. Therefore, we conclude that NOX4 plays a crucial role in inducing the recruitment of AMs by controlling ICAM1 expression in lung endothelial cells, which is responsible for resolving lung inflammation during acute S. aureus infection.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.221.2-222
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• 2003

Expressions of cellular adhesion molecules (CAMs) are closely related to the formation of early atherosclerosis, an age-dependent vascular disorder. However. previous research provided only limited and conflicted reports on age-related alterations of CAMs' expressions and even much less is known the modulation of CAMs by calorie restriction (CR), In this study, expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, P-selectin and platelet/endothelial cell adhesion molecule-1 (PECAM-1) in aorta and kidney were investigated by western blot and immuno-histochemical stain utilizing ad libitum (AL) and CR rat. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.1
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• pp.27-38
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• 2021

Excessive salt intake induces hypertension, but several gamma-aminobutyric acid (GABA) supplements have been shown to reduce blood pressure. GABA-salt, a fermented salt by L. brevis BJ20 containing GABA was prepared through the post-fermentation with refined salt and the fermented GABA extract. We evaluated the effect of GABA-salt on hypertension in a high salt, high cholesterol diet induced mouse model. We analyzed type 1 macrophage (M1) polarization, the expression of M1 related cytokines, GABA receptor expression, endothelial cell (EC) dysfunction, vascular smooth muscle cell (VSMC) proliferation, and medial thicknesses in mice model. GABA-salt attenuated diet-induced blood pressure increases, M1 polarization, and TNF-α and inducible nitric oxide synthase (NOS) levels in mouse aortas, and in salt treated macrophages in vitro. Furthermore, GABA-salt induced higher GABAB receptor and endothelial NOS (eNOS) and eNOS phosphorylation levels than those observed in salt treated ECs. In addition, GABA-salt attenuated EC dysfunction by decreasing the levels of adhesion molecules (E-selectin, Intercellular Adhesion Molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1]) and of von Willebrand Factor and reduced EC death. GABA-salt also reduced diet-induced reductions in the levels of eNOS, phosphorylated eNOS, VSMC proliferation and medial thickening in mouse aortic tissues, and attenuated Endothelin-1 levels in salt treated VSMCs. In summary, GABA-salt reduced high salt, high cholesterol diet induced hypertension in our mouse model by reducing M1 polarization, EC dysfunction, and VSMC proliferation.

• KSBB Journal
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• v.24 no.2
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• pp.122-130
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• 2009

Anti-angiogenic mechanism was examined for anti-obesity agents with the extract of P.radix, P.semen, S.hebra and C.furctus through anti-cell adhesion effect and western blot. Cell adhesion molecules, VCAM-1 was supressed with the order of P.radix (0.2 ppm, 125%) > P.semen (0.5 ppm, 100%) > S.hebra (5.0 ppm, 114%) > C. furctus (5.0 ppm, 111.8%), ICAM-1 was inhibited by P.radix (0.25 ppm, 130%) > P.semen (0.5 ppm, 100%) > S.hebra (5.0 ppm, 138%) > C. furctus (5.0 ppm, 66.7%), E-Selectin was also supressed P.radix (0.25 ppm, 100%) > P.semen (1.0 ppm, 128%) > S.hebra (5.0 ppm, 120%) > C. furctus (5.0 ppm, 100.7%). And signal molecules, VE-cadherin was supressed by P.radix and S.hebra, ${\beta}$-catenin was inhibited by P.radix, and Akt was supressed all these 4 kinds of natural products. These P.radix, P.semen, S.hebra and C.furctus were showed the possibility of anti-obesity agents based on anti-angiogenesis.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1152-1156
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• 2007

The Camella japonica flower(CJF) extract was studied for their anti-angiogenenic and anti-cell adhesion effect. CJF-extract inhibited the tube formation on human umbilical vein endotherial cells(HUVEC) with butanol extract by 70.2%, acetone extract by 54.2%, ethyl acetate extract by 37.0%, chloroform extract by 21.2%. Cell adhesion molecules were effectively suppressed at different concentration of CJF at 50, 100, 200 ug/well such as for intercellular adhesion molecule(ICAM) by 5.9%, 29.4% and 52.9%, for vascular cell adhesion molecule(VCAM) by 12.5%, 43.8% and 62.5%, for E-selectin by 7.1%, 21.4% and 35.7%, respectively. Signal molecules of vascular endotherial growth factor receptor 2(VEGFR2), ${/beta}$-catenin and PI3K are inhibited by different concentration of CJF at 10, 20 and 30 ${\mu}g/mL$ with western blot. Angiogenesis will be inhibited with suppressing NF-kB molecule resulted in signal molecules blocked by CJF. CJF will be useful materials for treatment of angiogenesis related diseases such as cancer, metastasis, rheumathioid arthritis and obesity.

• KSBB Journal
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• v.22 no.4
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• pp.249-254
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• 2007

Anti-angiogenesis and anti-cell adhesion effects were investigated with different dose of Camellia japonica leaf (CJL) extract for applying anti-cancer, anti-metastasis and anti-obesity. Cytotoxicity on HUVECs was very low at 200 ug/mL of CJL-extract. Anti-angiogenic ratio at increasing dose of 1.5 ug/mL, 3.0 ug/mL, 15 ug/mL and 30 ug/mL was showed 30.7%, 38.5%, 53.8%, and 70.0%, respectively. Also, anti-cell adhesion effect at concentration of $50{\mu}g{/well},\;100{\mu}g{/well}\;and\;200{\mu}g{/well}$ was expressed on E-selectin by 46.7%, 66.7%, and 86.76%, on VCAM-1, 23.0%, 61.5%, and 84.6%, and on ICAM-1, 11%, 55.5%, and 88.8%, respectively. For inquiring anti-angiogenesis mechanism, when western blot was performed with different dose of CJL extract, signal molecules of VEGFR-2, $\beta$-catenin and PI3-K were suppressed. As the signal transduction from VEGFR-2, $\beta$-catenin and PI3-K to NF-${\kappa}$B was interupted, angiogenesis could not be occurred causing not activated NF-kB. C. japonica leaf (CJL) is a useful herb for developing therapeutics of angiogenesis related diseases such as cancer, metastasis, rheumathioid arthritis and obesity.

• Korean Journal of Microbiology
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• v.47 no.4
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• pp.348-355
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• 2011

Staphylococcus aureus is a major human pathogen that is associated with various types of local and systemic infection. Staphylococcal protin A (SPA), a highly expressed surface component of S. aureus, may have a role in virulence such as activating inflammation and interfering with immune clearance. We examined the effect of recombinant SPA on inflammatory response in human HaCaT keratinocytes. The recombinant SPA protein was prepared using the pET-28a Vector System in Escherichia coli. The expression of pro-inflammatory related adhesion molecules and cytokines in HaCaT cells incubated for 6, 12, and 24 h with SPA (2 ${\mu}g$/ml) was analyzed by comparative RT-PCR or ELISA. The expression of E-selectin, ICAM-1, MCP-1, IL-6 and IL-8 was significantly increased in HaCaT from 6 to 24 h after treatment with SPA. SPA showed the effect on the adhesion-promoting ability of U937 monocytes to HaCaT cells. Our data demonstrate that SPA stimulates inflammatory response of HaCaT cells, implicating an important factor for exacerbation of skin inflammation of immunologic disease.

• Journal of Ginseng Research
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• v.38 no.4
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• pp.244-250
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• 2014

Background: Panax ginseng has distinct and impressive health benefits, such as improved blood pressure and immune system functioning. Rg3-enriched Korean Red Ginseng (REKRG) isolated from Korean Red Ginseng contains a high percentage of Rg3. Methods: In this study, we examined the effects of REKRG on endothelial cell nitric oxide synthase (eNOS) activation and adhesion molecules in endothelial cells and vascular function in rats. Results: REKRG dose-dependently increased eNOS phosphorylation and nitric oxide (NO) production in endothelial cells. In addition, REKRG markedly inhibited the tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-mediated induction of intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expressions in endothelial cells. REKRG improved endothelium-dependent vasorelaxation in the Wistar-Kyoto (WKY) rat and spontaneously hypertensive rats (SHRs) compared with controls. Furthermore, REKRG treatment for 6 weeks increased serum NO levels and reduced the mean aortic intima-media thickness compared with controls. Conclusion: Taken together, these results suggest that REKRG increased vascular function and improved immune system functioning. Therefore, REKRG is a very useful food for preventing or improving various cardiovascular diseases.

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.406-411
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• 2005

Fermented materials with enterobacteria isolated from fusiform fish, have strong anti-angiogenesis effect and anti-cell adhesion effect. PLM-f74 got from 74th fraction of size exclusion chromatography from fermented material, showed strong anti-cell adhesion effect between HUVECs and U937 monocytic cell. Adhesion of U937 cell to HUVEC stimulated with IL-1b was clearly inhibited by PLM-f74 in a dose-dependent manner by 12.1, 21.2, 50.9, and 78.2%, when U937 cells treated with each of the PLM-f74 and stimulated with PMA (100 mg/L) was added onto untreated and unstimulated HUVECs, adhesion was observed by 15.8, 31.9, 70.8, and 102%, when both cell types were pretreated with PLM-f74, the adhesion was prominently decreased by 83.7, 99.2, 110, and 120.8%, with 0.74, 3.7, 7.4, and 18.5ug/mL of PLM-f74, respectively. PLM-f74, also, reduced IL-1-stimulated HUVEC expression of adhesion molecules, VCAM-1, ICAM-1, and E-selectin dose-dependently by ELISA method.

• Journal of Haehwa Medicine
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• v.27 no.2
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• pp.11-20
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• 2018

Objectives : Coronary and cerebrovascular disease with high mortality is a major factor in arteriosclerosis. Pro-inflammatory cytokines damage vascular endothelial cells, leading to vascular inflammation. These vascular inflammation can build up cholesterol and thrombus to cause atherosclerosis. Methods : In this study, we researched the effect of ChungHyul-Plus for vascular inflammation in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$). Change in mRNA expression of inflammatory cytokines (CCL5, CXCL8, CX3CL1, and MCP-1), cell adhesion molecules (VCAM-1 and ICAM-1), and anti-inflammation modulators (KLF2 and eNOS) were quantified by qRT-PCR. Results : ChungHyul-Plus decreased expression of inflammatory cytokines and cell adhesion molecules and increased anti-inflammation modulators expression in $TNF-{\alpha}$ stimulated HUVECs. Conclusions : These results suggest that ChungHyul-Plus can be used in the treatment and prevention of vascular inflammation and arteriosclerosis.