• Journal of the Society of Cosmetic Scientists of Korea
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• v.45 no.2
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• pp.117-129
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• 2019

In this study Anti-inflammatory activity was investigated for the extract of Prunus pendula for. ascendens (Makino) Ohwi by monitoring nitric oxide (NO) production in LPS-stimulated RAW 264.7 murine macrophage cells. The P. pendula ethyl acetate (EtOAc) fraction showed to decrease the NO synthesis by 76.3% at $100{\mu}g/mL$ concentration. The inhibition occurred in a dose-dependent manner without causing cell toxicity. The EtOAc fraction also inhibited the production of $PGE_2$, $IL-1{\beta}$, IL-6 and expression of iNOS, COX-2 protein in dose-dependent manner. From the phytochemical study to isolate the active constituents, five known compounds were identified, which are ursolic acid (1), prunasin (2), methyl p-coumarate (3), kaempferol (4), astragalin (5). All of the compounds 1 - 5 were isolated for the first time from the P. pendula. Among the isolates, the flavonoids 4 and 5 were verified to inhibit NO production with high efficiency. These results suggested that extract of P. pendula leaves could be useful as anti-inflammatory agents in pharmaceutical or cosmetic applications.

• IMMUNE NETWORK
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• v.24 no.2
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• pp.3.1-3.23
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• 2024

Cigarette smoke extract (CSE)-treated mouse airway epithelial cells (MAECs)-derived exosomes accelerate the progression of chronic obstructive pulmonary disease (COPD) by upregulating triggering receptor expressed on myeloid cells 1 (TREM-1); however, the specific mechanism remains unclear. We aimed to explore the potential mechanisms of CSE-treated MAECs-derived exosomes on M1 macrophage polarization and pyroptosis in COPD. In vitro, exosomes were extracted from CSE-treated MAECs, followed by co-culture with macrophages. In vivo, mice exposed to cigarette smoke (CS) to induce COPD, followed by injection or/and intranasal instillation with oe-TREM-1 lentivirus. Lung function and pathological changes were evaluated. CD68⁺ cell number and the levels of iNOS, TNF-α, IL-1β (M1 macrophage marker), and pyroptosis-related proteins (NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, cleaved-caspase-1, gasdermin D [GSDMD], and GSDMD-N) were examined. The expression of maternally expressed gene 3 (MEG3), spleen focus forming virus proviral integration oncogene (SPI1), methyltransferase 3 (METTL3), and TREM-1 was detected and the binding relationships among them were verified. MEG3 increased N6-methyladenosine methylation of TREM-1 by recruiting SPI1 to activate METTL3. Overexpression of TREM-1 or METTL3 negated the alleviative effects of MEG3 inhibition on M1 polarization and pyroptosis. In mice exposed to CS, EXO^-CSE further aggravated lung injury, M1 polarization, and pyroptosis, which were reversed by MEG3 inhibition. TREM-1 overexpression negated the palliative effects of MEG3 inhibition on COPD mouse lung injury. Collectively, CSE-treated MAECs-derived exosomal long non-coding RNA MEG3 may expedite M1 macrophage polarization and pyroptosis in COPD via the SPI1/METTL3/TREM-1 axis.

• Microbiology and Biotechnology Letters
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• v.43 no.1
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• pp.45-55
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• 2015

This study was carried out to demonstrate the anti-inflammatory effect of tuna oil (TO) using LPS-induced inflammation responses and mouse models. First, nitric oxide (NO) and pro-inflammatory cytokines levels were suppressed up to 50% with increasing concentrations of TO without causing any cytotoxicity. Also, the expression of a variety of proteins, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB), was suppressed in a dosedependent manner by treatment with TO. Furthermore, TO also inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 protein kinase (p38). Moreover, in in vivo testing the formation of ear edema was reduced at the highest dose tested compared to that in the control, and a reduction of ear thickness and the number of mast cells was observed in histological analysis. In acute toxicity test, no mortalities occurred in mice administrated 5,000 mg/kg body weight of TO over a two-week observation period. Our results suggest that TO has a considerable anti-inflammatory property through the suppression of inflammatory mediator productions and that it could prove to be useful as a potential anti-inflammatory therapeutic material.

• Journal of Life Science
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• v.25 no.7
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• pp.801-809
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• 2015

Homotypic cell adhesion (homotypic aggregation) in activated monocytes plays a central role in physiological and pathological processes including inflammatory responses, differentiation and migration. The extract of the Prunus mume Sieb. et Zucc. fruit (Maesil) has potential benefits to human health; such as anti-viral, anti-microbial, and anti-cancer activities. Indeed, Maesil extract may modulate inflammatory responses via interference with homotypic aggregation in monocytes. In the present study, the molecular mechanisms underpinning the therapeutic efficacy of Maesil extract in inflammatory diseases were investigated. It was found that Maesil extract inhibited homotypic aggregation in lipopolysaccharide (LPS)-activated monocytes. This was mediated by reduction of nitric oxide (NO) production, partly via inhibition of inducible nitric oxide synthase (iNOS) expression in LPS-activated THP-1 cells. It was confirmed that NO inhibition is a key mechanism in Maesil induced blockade of monocyte aggregation through identification of reversal of this inhibitory effect by the NO-producing agent S-nitroso-N-acetyl penicillamine (SNAP). In addition, Maesil extract significantly attenuated LPS-induced IκB-α phosphorylation and NF-κB translocation into the nucleus. In conclusion, Maesil extract exerts anti-inflammatory effects via inhibition of homotypic aggregation of LPS-activated monocytes through mechanisms involving the suppression of NO production and NF-κB activity, suggesting Maesil extract as a potential therapeutic candidate for the prevention and treatment of chronic inflammatory diseases.

• Food Science and Preservation
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• v.24 no.8
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• pp.1149-1157
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• 2017

Inflammation is the first response of the immune system to infection or irritation in our body. The use of medicinal plants has been widely applied as an alternative source for drug development. One of marine natural resources, the anti-inflammatory effect of Ishige sinicola ethanol extract (ISEE), was evaluated by using LPS-induced RAW 264.7 cell and mice model. As a result, the production of nitric oxide (NO) and pro-inflammatory cytokines (IL-6, IL-$1{\beta}$, TNF-${\alpha}$) were inhibited with increasing concentration of ISEE without any cytotoxicity. Furthermore, ISEE suppressed the expression of not only inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-${\kappa}B$) p65, and mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK) 1/2, p38, and c-Jun N-terminal kinase (JNK) in a dose-dependent manner. In mice ear edema test, the formation of edema was reduced at the highest dosage of ISEE and the reduction of the number of infiltrated mast cells was observed in histological analysis. These results indicate that ISEE has a potent anti-inflammatory activity and can be used as a pharmaceutical material for many kinds of inflammatory disease.

• Lingua Humanitatis
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• v.7
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• pp.271-289
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• 2005

Dans cet article, nous discutons de certains $probl{\grave{e}}mes$ syntaxiques en ayant recours $\grave{a}$ la $th{\acute{e}}orie$ linguistique de Milner. Nous remettons en question $l'ind{\acute{e}}pendance$ et $l'identit{\acute{e}}$ de la structure syntaxique, la relation entre le plan syntaxique et le plan lexical, le $caract{\grave{e}}re$ de la $g{\acute{e}}om{\acute{e}}trie$ de la syntaxe, etc.. La discussion est non seulement linguistique mais aussi interdisciplinaire et ${\acute{e}}pist{\acute{e}}mologique$, dans la mesure $o{\grave{u}}$ nous examinons la nature de $l'entit{\acute{e}}$ syntaxique et la $m{\acute{e}}thode$ "scientifique" de la syntaxe qui donne $acc{\grave{e}}s$ $\grave{a}$ $l'entit{\acute{e}}$ syntaxique. Selon Milner, il faut distinguer la place du terme lexical avec la position syntaxique qui est $l'entit{\acute{e}}$ syntaxique. La $premi{\grave{e}}re$ n'est pas syntaxique $\grave{a}$ strictement parler, mais elle, observable contrairement $\grave{a}$ la seconde, sert $\grave{a}$ conjecturer la dimension syntaxique, $c'est-\grave{a}-dire$ le $syst{\grave{e}}me$ positionnel. Le dispositif $th{\acute{e}}orique$ dans la $th{\acute{e}}orie$ linguistique de Milner n'est rien d'autre que l'ensemble des propositions qui permet, en absence d'observatoire, de conjecturer le $syst{\grave{e}}me$ positionnel sur la base du $syst{\grave{e}}me$ des places. Dire $l'ind{\acute{e}}pendance$ de la structure syntaxique revient $\grave{a}$ dire qu'il y a une coupure entre le $syst{\grave{e}}me$ positionnel et le $syst{\grave{e}}me$ des places. Autrement dit, sans cette coupure, on ne peut parler de $l'ind{\acute{e}}pendance$ de la structure syntaxique. Ainsi $distingu{\acute{e}}s$, les deux $syst{\grave{e}}mes$ en cause se mettent en relation soit naturels soit non naturels ou par distorsion $d'apr{\grave{e}}s$ Milner. La relation naturelle est une relation lexico-syntaxique $n{\acute{e}}e$ au moment $o{\grave{u}}$ un terme lexical occupe une position syntaxique dont la $cat{\acute{e}}gorie$ est identique $\grave{a}$ celle de son occupant. A la $diff{\acute{e}}rence$ de cette relation d'occupation naturelle $suppos{\acute{e}}e$ chez Milner comme une tendance du langage naturel, la relation d'occupation non naturelle est "paradoxale" dans le sens $o{\grave{u}}$ elle est produite dans la rencontre plus ou moins "anomale" entre l'occupant lexical et $l'occup{\acute{e}}$ syntaxique. Le $degr{\acute{e}}$ de l'anomalie qu'une langue autorise peut ${\hat{e}}tre$ $mesur{\acute{e}}$ empiriquement et doit ${\hat{e}}tre$ $vari{\acute{e}}$ en fonction de la langue $concern{\acute{e}}e$. Le $caract{\grave{e}re$ $g{\acute{e}}om{\acute{e}}trique$ de la syntaxe $am{\grave{e}}ne$ ${\grave{a}}$ remettre en cause, entre autres, $l'empiricit{\acute{e}}$ et la $mat{\acute{e}}rialit{\acute{e}}$ de la $g{\acute{e}}om{\acute{e}}trie$ syntaxique. En ce qui concerne ces sujets, nos $th{\grave{e}}ses$ sont les suivantes : la nature de la $g{\acute{e}}om{\acute{e}}trie$ syntaxique n'est pas a priori mais empirique ; la $g{\acute{e}}om{\acute{e}}trie$ de la syntaxe peut et doit ${\hat{e}}tre$ construite $\grave{a}$ l'aide de la logique "empirique".

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.9
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• pp.1139-1145
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• 2006

In this study, antioxidant activities of enzymatic and methanolic extracts from E. cava stem and leave were evaluated by measuring the scavenging activities on 1,1 diphenyl 2 picrylhydrazyl (DPPH), hydroxyl radical, hydrogen peroxide and the inhibitory effects on DNA damage induced by oxidative stress of cells. Enzymatic extracts were prepared by enzymatic hydrolysis of both stem and leave using food grade five different carbohydrases (Viscozyme, Celluclast, AMG, Termamyl, Ultraflo) and five proteases (Protamex, Kojizyme, Neutrase, Flavourzyme, Alcalase). The enzymatic extracts were lower than methanolic extracts in polyphenol contents, but higher in extraction yield by approximately 30%. The enzymatic extracts were superior to methanolic extracts in DPPH and H2O2 scavenging activities and DNA damage protective effect. There were no significant antioxidant activity difference between stem and leave, but the extracts of leave were relatively better than those of stem. In this study it is suggested that E. cava stem as well as its leave would be a good raw materials for antioxidants compound extraction and enzymatic hydrolysis would be a good strategy to prepare antioxidant extracts from seaweeds.

• The Journal of Korean Medicine
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• v.34 no.1
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• pp.116-135
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• 2013

Objectives: This study was intended to clarify how Jakyakkamchobuja-tang (hereinafter referred to JKBT) affects mice of C57BL/10 whose osteoarthritis was induced by papain. Methods: Osteoarthritis was induced in mice by injecting papain in the knee joint. Mice were divided into 4 groups (n=6). The normal group were not treated at all whereas the control group (OAC-control) were induced for osteoarthritis by papain and oral medicated with 200 ul of physiological saline per day. The positive comparison group (OAC-$Joins^{(R)}$) were injected with papain and after 7 days, 100 mg/kg of $Joins^{(R)}$ were medicated with 200 ul of physiological saline mixed. The experimental group (OAC-JKBT) were injected with papain and after 7 days were medicated with 400 mg/kg of JKBT mixed with 200 ul of physiological saline. OAC-$Joins^{(R)}$ and OAC-JKBT were oral medicated for each substance for a total of 4 weeks, once per day. After experiments (from 1 week after injection of papain to 4 weeks elapsed), the function of liver and kidney, inflammation cytokine values within serum, degree of revelation for inflammation cytokine genes, immune cells within blood, metabolism of arachidonic acid and amount of cartilage were measured and histopathological variations for knee joint structures were observed. Results: Functions of liver and kidney were not affected. IL-$1{\beta}$ (interleukin-$1{\beta}$), MCP-1 (monocyte chemoattractant protein-1) and TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$) were significantly reduced and IL-6 (interleukin-6) was also reduced but not significantly. After analyzing inflammation cytokine in joints with mRNA (messenger ribonucleic acid), revelation of IL-6, TNF-${\alpha}$, COX-2 (cyclooxygenase-2) and iNOS-II (inducible nitric oxide synthase-II) were all significantly reduced. Revelation of IL-$1{\beta}$ gene was also reduced but not significantly. Neutrophil for WBC (white blood cell) within serum was significantly reduced; monocyte was also reduced but not significantly. PGE2 (prostaglandin E2), TXB2 (thromboxane B2) were significantly reduced and LTB4 (leukotriene B4) was also reduced but not significantly. Destruction of cartilage on micro CT (computed tomography)-arthrography was reduced but had no significant differences. In terms of histopathology, infiltration of inflammation, proliferation of synovial membrane, subsidence of cartilage and bone due to penetration of excessive formation of synovial cell and destruction of cartilage were small (H&E (hematoxylin and eosin), safranine O staining). Conclusions: Based on these results, Jakyakkamchobuja-tang (JKBT) is believed to be useful for suppressing the progress of osteoarthritis and its treatments because of its anti-inflammatory effects and alleviation of pain with histopathological effective efficacy.

• Journal of the Korean Applied Science and Technology
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• v.34 no.2
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• pp.189-202
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• 2017

This study was designed to examine the in vitro antioxidant and anti-inflammatory effects of kohlrabi (Brassica oleracea var. gonglodes) extract. Kohlrabi was extracted using 70% ethanol and then fractionated sequentially with n-hexane, ethyl acetate and butanol. Antioxidative ability was evaluated by bioassays using total polyphenol contents and ABTS (2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid diammonium salt) radical scavenging activity. Ethyl acetate fraction of kohlrabi was best on total polyphenol contents ($27.33{\pm}0.26mg\;GAE/g$) and ABTS radical scavenging effects ($IC_{50}\;172.9{\pm}1.6{\mu}g/mL$).For the anti-inflammatory activity in RAW 264.7 cells, the EtOAc fraction showed the highest inflammatory effect. Dose response studies were performed to determine the inhibitory effect of EtOAc fraction of kohlrabi on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The EtOAc fraction of kohlrabi inhibited the NO and $PGE_2$ production and the protein level of iNOS and COX-2, and protein expression of pro-inflammatory cytokines (TNF-${\alpha}$, IL-6 and IL-$1{\beta}$), in a dose-dependent manner. These results suggest that kohlrabi has considerable potential as a ingredient with antioxidative and anti-inflammatory effects.

• Journal of Life Science
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• v.24 no.10
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• pp.1137-1143
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• 2014

Doxorubicin is a general chemotherapy drug widely used for a number of cancers. However, the correlation between endogenous nitric oxide ($NO^{\bullet}$) levels and chemoresistance to doxorubicin remains unclear. In this study, we investigated the effect of endogenous $NO^{\bullet}$ on the anticancer activity of doxorubicin in human colon cancer cell lines HCT116 and HT29 with different p53 status. The cells were treated with either doxorubicin alone or in combination with the $NO^{\bullet}$ synthase (NOS) inhibitor $N^G$-monomethyl-L-arginine (NMA). Doxorubicin differentially inhibited the growth of both the HCT116 (p53-WT) and HT29 (p53-MUT) cells, which was mitigated by cotreatment with NMA. Further studies revealed that inhibition of endogenous $NO^{\bullet}$ mitigated doxorubicin-induced apoptosis in the HCT116 and HT29 cells, as evidenced by apoptotic DNA fragmentation and the sub-G1 peak of apoptotic markers. Apoptosis was delayed in the HT29 cells, and its magnitude was greatly reduced, underscoring the importance of the modulation of p53 in the response. RT-PCR analysis revealed that doxorubicin down-regulated levels of inhibitors of the apoptosis family (cellular IAP-1 and-2). Collectively, these data show that induction of apoptosis by doxorubicin in human colon cancer cells is possibly related to modulation of endogenous $NO^{\bullet}$, the expression of the IAP family of genes, and the status of p53. The underlying mechanisms may represent potential targets for adjuvant strategies to improve the efficacy of chemotherapy for colon cancer.