• Journal of Biomedical and Translational Research
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• v.19 no.4
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• pp.92-102
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• 2018

The objectives of this study were to find out the plant to enhance immune activity among 42 kinds of foods frequently consumed by the Korean elderly consisting of 5 food groups and 5 wild plants. Each sample was assessed the immunoactive effect by measuring $NF-{\kappa}B/AP1$ gene expression, nitric oxide and cytokine production in $RAW-Blue^{TM}$ cell. Soybean sprouts of 47 plants showed the highest $NF-{\kappa}B/AP1$ gene expression at the level of $1.13{\pm}0.03$ (O.D. 650 nm) and Soritae, sweet potato, banana, apple, garlic, crown daisy, cabbage and Ailanthus altissima also had high activity of $NF-{\kappa}B/AP1$ gene in $RAW-Blue^{TM}$ cell stimulated by LPS. NO production of Ailanthus altissima was significantly higher than that of other plants and 16 plants of glutinous sorghum, black rice, Seoritae, Heuktae, sweet potato, banana, apple, garlic, mungbean sprouts, spinach, crown daisy, young pumpkin, cabbage, soybean sprouts, Actinidia arguta and Aster scaber were the next best activity. The above results selected 17 out of 47 plant samples. Moreover, soybean sprouts was significantly shown to increase $TNF-{\alpha}$ ($1,509.55{\pm}1.38pg/mL$) and $IL-1{\beta}$ ($54.56{\pm}1.08pg/mL$) cytokines in comparison with RAW-Blue cell stimulated by LPS. According to the results of in vitro evaluation, the ethanol extract of soybean sprout increased the production of immune-enhancing cytokines by proliferation of macrophages. In addition, $NF-{\kappa}B$ transcription factor activity and NO production ability were excellent, and it was selected as a material having excellent immunological activity.

• Tuberculosis and Respiratory Diseases
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• v.62 no.4
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• pp.299-307
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• 2007

Background: High mobility group box 1 (HMGB1) is a novel, late mediator of inflammation. This study compared the pro-inflammatory effects of LPS and HMGB1. The transcriptional factors that play an important role in mediating the HMGB1-induced stimulation of IL-8 were also evaluated. Methods: RAW264.7 cells were stimulated with either LPS (100 ng/ml) or HMGB1 (500 ng/ml). The $TNF-{\alpha}$, MIP-2 and $IL-1{\beta}$ levels in the supernatant were evaluated by ELISA at 0, 2, 4, 8, 12 and 24h after stimulation. An acute lung injury was induced by an injection of LPS (5 mg/kg) or HMGB1 (2.5 mg/kg) into the peritoneum of the Balb/c mice. The lung cytokines and MPO activity were measured at 4h (for LPS) or 24h (for HMGB1) after the injection. The transcriptional factor binding sites for NF-IL6, $NF-{\kappa}B$ and AP-1 in the IL-8 promoter region were artificially mutated. Each mutant was ligated with pIL-6luc and transfected into the RAW264.7 cells. One hour after stimulation with HMGB1 (500 ng/ml), the cell lysate was analyzed for the luciferase activity. Results: The expression of MIP-2, which peaked at 8h with LPS stimulation, increased sequentially until 24h after HMGB1 stimulation. An intraperitoneal injection of HMGB1, which induced a minimal increased in $IL-1{\beta}$ expression, provoked the accumulation of neutrophils the lung. A mutation of AP-1 as well as $NF-{\kappa}B$ in the IL-8 promoter region resulted in a lower luciferase activity after HMGB1 stimulation. Conclusion: The proinflammatory effects of HMGB1, particularly on IL-8, are mediated by both $NF-{\kappa}B$ and AP-1.

• Proceedings of the Korean Radioactive Waste Society Conference
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• 2005.06a
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• pp.137-144
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• 2005

Silica in primary system combines with an alkali grammatical particle metal and forms the zeolite layer which is hindering the heat transfer on the surface of the cladding. Zeolite layer becomes the cause of the damage in this way. The problems of the NPP's primary system have been issued steadily by EPRI. Through a series of experiments of the laboratory scale, we confirmed the applicability of NF membrane for silica removal, as silica rejection rate of NF membrane is about $60\;{\sim}\;70\%$ and boron rejection rate is about $10\;{\sim}\;20\%$. We accomplished a site experiment about four NF membranes manufactured by FilmTec and Osmonics Inc. In experiment using 400L of SFP water, when operation pressure is $10kg_{f}/cm^2$, we confirmed that the silica rejection rate of NF90-2540 manufactured by FilmTec Inc. is about $98\%$, boron rejection rate is about $43\%$. The silica rejection rate of NF270-2540 is about $38\%$, boron rejection rate is about $3.5\%$. Afterward, through additional experiments, such as long term characteristic experiments, we are going to design a optimum NF membrane system for silica removal.

• Journal of Life Science
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• v.32 no.11
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• pp.899-907
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• 2022

Quercetin is one of bio-flavonoids which are abundant in fruits and vegetables and has been reported to have various pharmacological potentials such as anti-oxidation, anti-inflammation, anti-cancer, and anti-virus effects. In the present study, the anti-inflammatory effects and its working molecular mecha- nism of quercetin were investigated in mouse macrophage RAW264.7 cells. Quercetin significantly inhibited nitric oxide (NO) production in a dose-dependent manner without affecting cell viability and decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 cells. In addition, quercetin decreased phosphorylation of p38, JNK, and ERK, and inhibited phosphorylation of NF-κB p65 protein and its inhibitor IκBα indicating that quercetin has the anti-inflammatory effects via regulation of MAPKs and NF-κB signaling pathway. We also detected expression changes of four kinds of pro-inflammatory cytokine genes (CSF2, IL-1β, IL-6, and TNF-α) with quantitative real-time PCR. The results showed that quercetin decreased the expression of four pro-inflammatory genes in LPS-stimulated RAW264.7 cells. Overall, our results showed that quercetin effectively suppressed inflammation responses induced by LPS in RAW264.7 cells via regulating MAPK and NF-κB pathway and down-regulating the expression of pro-inflammatory cytokine genes.

• Tuberculosis and Respiratory Diseases
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• v.65 no.6
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• pp.504-511
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• 2008

Background: Particulate matter may be toxic to human tissue. Ambient air particulate matter ${\leq}10{\mu}m$ in aerodynamic size ($PM_{10}$), which changes under different environmental conditions, is a complex mixture of organic and inorganic compounds. The Asian dust event caused by meteorological phenomena can also spread unique particulate matter in affected areas. We evaluated production of ROS, $TGF-{\beta}$, fibronectin, and $NF{\kappa}B$ by exposing normal epithelial cells to Asian dust particulate matter. Methods: Bronchial epithelial cells were exposed to 0, 50, ${\leq}100{\mu}g/ml$ of a suspension of $PM_{10}$ for 24 h. ROS were detected by measurement of DCF release from DCF-DA by FACScan. $TGF-{\beta}$, fibronectin, and $NF{\kappa}B$ were detected by western blotting. Results: $PM_{10}$ exposure increased the expression of $TGF-{\beta}$, fibronectin, and $NF{\kappa}B$. ROS production and $TGF-{\beta}$ levels were significantly higher with 50 or ${\leq}100{\mu}g/ml$ $PM_{10}$. Fibronectin and $NF{\kappa}B$ production were significantly higher after ${\leq}100{\mu}g/ml$ of $PM_{10}$. Conclusion: $PM_{10}$ from Asian dust particles might have fibrotic potential in bronchial epithelial cells via ROS induction after $PM_{10}$ exposure.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.4
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• pp.239-246
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• 2003

The expression of cyclooxygenase-2 (COX-2) is a characteristic response to inflammation and can be inhibited with sodium salicylate. $TNF-{\alpha}$ plus $IFN-{\gamma}$ can induce extracellular signal-regulated kinase (ERK), IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation. The inhibition of the ERK pathway with selective inhibitor, PD098059, blocked cytokine-induced COX-2 expression and $PGE_2$ release. Salicylate treatment inhibited COX-2 expression induced by $TNF-{\alpha}$/$IFN-{\gamma}$ and regulated the activation of ERK, IKK and $I{\kappa}B$ degradation and subsequent NF-${\kappa}B$ activation in MC3T3E1 osteoblasts. Furthermore, antioxidants such as catalase, N-acetyl-cysteine or reduced glutathione attenuated COX-2 expression in combined cytokines-treated cells, and also inhibited the activation of ERK, IKK and NF-${\kappa}B$ in MC3T3E1 osteoblasts. In addition, $TNF-{\alpha}$/$IFN-{\gamma}$ stimulated ROS release in the osteoblasts. However, salicylate had no obvious effect on ROS release in DCFDA assay. The results showed that salicylate inhibited the activation of ERK and IKK, $I{\kappa}B$ degradation and NF-${\kappa}B$ activation independent of ROS release and suggested that salicylate exerts its anti-inflammatory action in part through inhibition of ERK, IKK, $I{\kappa}B$, $NF-{\kappa}B$ and resultant COX-2 expression pathway.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.144-152
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• 2017

Background: The ubiquitin-proteasome system (UPS) is an important pathway of proteolysis in pathologic hypertrophic cardiomyocytes. We hypothesize that MG132, a proteasome inhibitor, might prevent hypertrophic cardiomyopathy (CMP) by blocking the UPS. Nuclear factor kappa-light-chain-enhancer of activated B cells ($NF-{\kappa}B$) and androgen receptor (AR) have been reported to be mediators of CMP and heart failure. This study drew upon pathophysiologic studies and the analysis of $NF-{\kappa}B$ and AR to assess the cardioprotective effects of MG132 in a left ventricular hypertrophy (LVH) rat model. Methods: We constructed a transverse aortic constriction (TAC)-induced LVH rat model with 3 groups: sham (TAC-sham, n=10), control (TAC-cont, n=10), and MG132 administration (TAC-MG132, n=10). MG-132 (0.1 mg/kg) was injected for 4 weeks in the TAC-MG132 group. Pathophysiologic evaluations were performed and the expression of AR and $NF-{\kappa}B$ was measured in the left ventricle. Results: Fibrosis was prevalent in the pathologic examination of the TAC-cont model, and it was reduced in the TAC-MG132 group, although not significantly. Less expression of AR, but not $NF-{\kappa}B$, was found in the TAC-MG132 group than in the TAC-cont group (p<0.05). Conclusion: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis. However, $NF-{\kappa}B$ expression levels were not related to UPS function.

• BMB Reports
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• v.39 no.5
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• pp.618-625
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• 2006

The infiltration of both monocyte and activated T cells in the skin is one of critical steps in the development of UVB-induced inflammation. Upregulation of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1) on the surface of keratinocytes plays an important role in this process. In this study, we examined the molecular mechanism responsible for UVB-induced expression of ICAM-1 and subsequent monocyte adhesion by keratinocyte. We observed that (1) UVB induced protein and mRNA expression of ICAM-1 in a dose- and time-dependent manner in human keratinocyte cell HaCaT; (2) UVB induced the translocation of NF-kappaB and inhibition of NF-kappaB by NF-kappaB inhibitors suppressed UVB-induced mRNA and protein expression of ICAM-1; (3) UVB increased the intracellular level of reactive oxygen species (ROS) by HaCaT cells; (4) UVB-induced increase of intracellular ROS level was suppressed by pre-treatment with diphenyl iodonium (DPI) and N-acetyl cysteine (NAC); and (5) inhibition of UVB-induced ROS production by DPI or NAC suppressed UVB-mediated translocation of NF-kappaB, expression of ICAM-1 and subsequent monocyte adhesion in HaCaT cells. These results suggest that UVB-induced ROS is involved in the translocation of NF-kappaB which is responsible for expression of ICAM-1 and subsequent increased monocyte adhesion in human keratinocyte.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.1
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• pp.28-35
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• 2008

Purpose: The nitric oxide (NO) release by inducible nitric oxide synthase (iNOS) is the key events in macrophage response to lipopolysaccharide (LPS) which is suggested to be a crucial mediator for inflammatory and innate immune responses. NO is an important mediator involved in many host defense action and may also lead to a harmful host response to bacterial infection. However, given the importance of iNOS in a variety of pathophysiological conditions, control of its expression and signaling events in response to LPS has been the subject of considerable investigation. Materials and Methods: The Raw264.7 macrophage cell line was used to observe LPS-stimulated iNOS expression. The expression of iNOS is observed by Western blot analysis and real-time RT-PCR. Protein kinase C $(PKC)-{\alpha}$ overexpressing Raw264.7 cells are established to determine the involvement of $PKC-{\alpha}$ in LPS-mediated iNOS expression. $NF-{\kappa}B$ activity is measured by $I{\kappa}B{\alpha}$ degradation and $NF-{\kappa}B$ luciferase activity assay. Results: We found that various PKC isozymes regulate LPS-induced iNOS expression at the transcriptional and translational levels. The involvement of $PKC-{\alpha}$ in LPS-mediated iNOS induction was further confirmed by increased iNOS expression in $PKC-{\alpha}$ overexpressing cells. $NF-{\kappa}B$ dependent transactivation by LPS was observed and $PKC-{\alpha}$ specific inhibitory peptide abolished this activation, indicating that $NF-{\kappa}B$ activation is dependent on $PKC-{\alpha}$. Conclusion: Our data suggests that $PKC-{\alpha}$ is involved in LPS-mediated iNOS expression and that its downstream target is $NF-{\kappa}B$. Although $PKC-{\alpha}$ is a crucial mediator in the iNOS regulation, other PKC isozymes may contribute LPS-stimulated iNOS expression. This finding is needed to be elucidated in further study.

• Journal of Acupuncture Research
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• v.24 no.2
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• pp.1-14
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• 2007

목적 : 이 연구는 Vipera lebetina turanica의 사독약침파(蛇毒藥鍼波)(Snake venom toxin, SVT)이 in vitro에서 $NF-{\kappa}B$의 활성억제와 apoptosis 관련 단백질의 발현 조절을 통하여 세포자멸사(Apoptosis)를 유도하는지 in vivo에서 또한 전립선 암세포주인 PC-3 세포의 성장을 억제하는지 살펴보고자 하였다. 방법 : SVT를 처리한 후 PC-3의 성장억제를 관찰하기 위해 WST-1 assay, CCK-8 assay를 시행하였고，Apoptosis evaluation에는 DAPI, TUNEL staining assay를 시행하였으며，Apoptosis regulatory proteins의 변화 관찰에는 western blot analysis를 시행하였고，apoptosis와 연관된 $NF-{\kappa}B$의 활성 변화를 관찰하기 위해 EMSA시행하였으며，SVT의 핵내이동을 관찰하기 위해 Immunofluorescence Staining, Confocal immunocytochemistry를 시행하였으며，전립암세포의 종양형성에는 흉선을 제거한 쥐에 Tumorigenecity study를 시행하였다. 결과 : PC-3 세포에 SVT를 처리한 후，전립선 암세포의 성장，Apoptosis의 유발，Apoptosis관련 단백질의 발현，$NF-{\kappa}B$의 활성，SVT의 PC-3세포 핵내 이동여부 및 흉선제거 후 PC-3 세포를 이식한 쥐의 종양형성과정에 미치는 영향을 관찰하여 다음과 같은 결과를 얻었다. 1. PC-3 세포에서 SVT를 처리한 후 세포성장이 억제되고，세포자멸사가 유도되며，조절인자인 p53, caspase-3, -9는 증가되었고，Bcl-2는 감소되었다. 2. PC-3 세포에서 SVT를 처리한 후 $NF-{\kappa}B$의 활성이 유의하게 감소되었다. 3. DAPI로 염색된 상태에서 SVT가 PC-3 세포의 핵내로 이통되는 것이 관찰되었다. 4. 흉선제거 후 전립선 암세포주를 이식한 쥐에서 SVT를 피내로 주입한 결과 전립선암의 크기와 무게가 유의하게 감소하였다. 결론 : 이상의 결과는 SVT가 $NF-{\kappa}B$의 활성 억제를 통하여 인간 전립선암세포주인 PC-3의 세포자멸사를 유발함으로써 증식억제 효과가 있음을 입증한 것이며，이를 재확인한 생체 연구에서의 긍정적인 결과는 향후 SVT의 전립선암의 예방과 치료에 대한 효과적인 치료제 개발에 초석이 될 것으로 기대된다.