• The korean journal of orthodontics
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• v.28 no.4 s.69
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• pp.611-626
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• 1998

Cytokines are intercellular peptide mediators that regulate homeostasis and host defense reactions in living body. Of the diversity of cytokines in terms of biological accomplishment, interleukin $1-{\beta}$($IL-1{\beta}$) and tumor necrosis factor(TNF) are the most conspicuous cytokines with a wide variety of effects on cells involved in inflammatory and immune responses, and likely to be involved in the inflammatory pathogenesis of oral tissue as well. The present study was designed to explicate the role of $IL-1{\beta}$ on inflammatory revelation of oral tissues in mice biochemically. In the Induced arthritis by injection of 10${\mu}g$ LPS shown the relaese of 0.93 ${\mu}g$ $IL-1{\beta}$/joint with a peak at at 4-5 h. and diminished at 24t and the release of $TNF_{\alpha}$ of 1.25 ${\mu}g$/joint with a peak at 2-3h and diminished at 6h. After injection of th $IL-1{\beta}$ into the joint, the mumber of leucocytes proliferated with a peak at 4-5h and diminished at 36h and the loss of proteoglycan showed with maximum at 15-30h. After injection of $IL-1{\beta}$ into the oral tissue, cycloosygenase metabolites ($PGE_2$) accumulated in the oral tissue with dose dependant. These elucidated $IL-1{\beta}$ to be inflammatory mediator in the early phase of its pathogenesis. Intraoral injection of recombinant $IL-1{\beta}$ induced the proliferation of leukocytes in situ. $IL-1{\beta}$ took an pertinent part in the development of inflammation and the succession of cellular infiltration. The results exemplify that $IL-1{\beta}$ plays a significant role in mediating inflammatory response induced by LPS in oral tissue, the inflammatory response is regulated by $IL-1{\beta}$ at an acute phase of pathogenesis.

• Tuberculosis and Respiratory Diseases
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• v.39 no.4
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• pp.304-309
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• 1992

Background: The alveolar macrophage may metabolize arachidonic acid through cyclooxygenase- and lipoxygenase- catalyzed pathways to produce a variety of metabolites of arachidonic acid. The production of these metabolites of arachidonic acid may enhance the defensive ability of the challenged lung. However, continued stimulation with the consequent production of proinflammtory metabolites of arachidonic acid, may ultimately enhance the disease process by contributing to chronic bronchoconstriction, fibrosis, and the persistent release of toxic oxygen species. Silicosis is an example of a disease process resulting from chronic exposure of the lung to foreign particles. This study was carried out to evaluate the changes of arachidonic acid metabolites from macrophages in experimental silicosis. Methods: We measured $PGE_2$, and $LTB_4$ in cultured macrophages taken from rats by radioimmunoassay at 24 and 48 hours after stimulation by silica dust, natural carbon dust, lipopolysaccharide, calcium ionophore (A23187) and medium (RPMI) as a control. For the experimental silicosis, 50 mg silica in 0.5 ml saline was administered intratracheally into the rat and grown to 20 weeks and measured $PGE_2$, and $LTB_4$ in the cultured macrophages lavaged from that rat. The used stimulants were the same as above. Results: 1) The amount of $PGE_2$ in the cultred macrophages from normal rat was significantly decreased in the group which was stimulated with silica dust for 48 hours compare with control non-stimulated group. 2) In the experimental silicosis group, $PGE_2$, release in cultured macrophages after 48 hours incubation with silica and natural carbon dust tended to be lower than those of non-stimulated group. 3) There were marked changes of $LTB_4$ in the groups of normal rats which were incubated with silica for 24, 48 hours and natural carbon for 48 hours compared with non-stimulated group. 4) In the experimental silicosis group, the release of $LTB_4$ was significantly increased macrophages cultured with silica and natural carbon dust after 24 and 48 hours incubation compared with non-stimulated group. Conclusion: The results of these studies suggest that the in vitro exposure of rat alveolar macrophge to silica and coal dust results in an alteration in alveolar macrophage metabolism of arachidonic acid that may promote an inflammatory reaction in lung tissue.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.47 no.1
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• pp.75-84
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• 2021

In this study, we investigated inhibitory effect of Tripeptide against particulate matter (PM)-induced damage in human keratinocytes. PM-induced cell death was inhibited by Tripeptide and the activity of aryl hydrocarbon receptor (AhR) also inhibited by Tripeptide resulting in reduced expression of its downstream targets, cytochrome P450 family 1 subfamily A member 1 (CYP1A1) and cyclooxygenase-2 (COX-2), which are responsible for toxic metabolites production and inflammation. Furthermore, PM-induced expressions of pro-inflammatory cytokines, matrix metalloproteinase-1 (MMP-1) and apoptosis-related factors were decreased by anti-oxidant activity of Tripeptide. From these results, it has been shown that the Tripeptide has protective effect against PM-induced skin damage not only through the inhibiting of keratinocyte death but also through the inhibiting the secretion of several damage-inducing factors to adjacent skin tissue. And the results suggested that Tripeptide with anti-pollution effect could be applied as a new functional cosmetic material.

• Journal of Life Science
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• v.30 no.4
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• pp.352-358
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• 2020

Red yeast rice has been extensively used as a food and traditional medicine for thousands of years in Korea. Monascus produces many secondary metabolites during its growth, including pigments, monacolins, and γ-aminobutyric acid. Some metabolites, specifically monacolin K, γ-aminobutyric acid, and dimerumic acid, have been reported to lower cholesterol and blood pressure because of certain antioxidant effects. This study investigated the total phenolic content of ethanol extract from red yeast rice fermented with Monascus sp. BHN-MK and its anti-inflammatory effect on LPS-stimulated RAW 264.7 macrophage cells. To assess its anti-inflammatory effect, the inhibitory activity of the ethanol extract on LPS-induced NO production and expression levels of iNOS and COX-2 proteins in macrophage cells were measured. Its total polyphenol content was higher than that of ordinary non-fermented rice. Its NO production inhibition activity was comparable to that of the negative control group treated with LPS at a concentration of 400 ㎍/ml. Western blot revealed a significant decrease in the inhibition of iNOS and COX-2 protein expression at concentrations of 400 and 800 ㎍/ml, respectively. Red yeast rice ethanol extracts exerted the strongest anti-inflammatory effects. The results indicate that red yeast rice could be used as a functional cosmetic and anti-inflammatory material.

• Journal of Nutrition and Health
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• v.24 no.2
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• pp.97-103
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• 1991

The increase in alcohol consumption level has been noticed in Korea recently. Alcohol appreciably inhibits cell mediated immunity and this may contribute to the high prevalence of serious infection such as pulmonary tuberculosis among alcoholic subjects. The present study was undertaken to examine the effect of ethanol on the cyclooxygenase metabolites of human monocyte in vitro. Monocytes were activated with 800 units of gamma interferon(IFN-${\gamma}$) for 3 days following apply of Ficool-hypaque density gradient and gelatin coated flasks for separation of monocytes. Ethanol with addition of 100mM, 300mM and 600 mM for 30 minutes to 106 monocytes with/without previous IFN-${\gamma}$ treatment caused a dose dependent decrease in the production of thromboxane B2, 6-keto-PGE1$\alpha$ and PGE2 by radioimmunoassay at 6 hours after ethanol treatment. Quite different from the findings after 6 hours there was dose dependent increase in three prostaglandins without IFN-${\gamma}$ treatment after 24 hours of incubation. With previous treatment of IFN-${\gamma}$ reduced productions of three prostaglandins at 24 hours than control is spite of ethanol stimjulation. These findings show that IFN-${\gamma}$ can inhibit alcohol induced derangement of arachidonic acid metabolism of monocytes.

• Journal of Microbiology and Biotechnology
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• v.16 no.11
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• pp.1791-1798
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• 2006

When ginsenoside Rg5, a main component isolated from red ginseng, was incubated with three human fecal microflora for 24 h, all specimens showed hydrolyzing activity: all specimens produced ginsenoside Rh3 as a main metabolite, but a minor metabolite $3{\beta},12{\beta}$-dihydroxydammar-21(22),24-diene (DD) was observed in two specimens. To evaluate the antiallergic effect of ginsenoside Rg5 and its metabolites, the inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 against RBL-2H3 cell degranulation, mouse passive cutaneous anaphylaxis (PCA) reaction induced by the IgE-antigen complex, and mouse ear skin dermatitis induced by 12-O-tetradecanoilphorbol-13-acetate (TPA) were measured. Ginsenosides Rg5 and Rh3 potently inhibited degranulation of RBL-2H3 cells. These ginsenosides also inhibited mRNA expression of proinflammatory cytokines IL-6 and $TNF-{\alpha}$ in RBL-2H3 cells stimulated by IgE-antigen. Orally and intraperitoneally administered ginsenoside Rg3 and orally administered ginsenoside Rg5 to mice potently inhibited the PCA reaction induced by IgE-antigen complex. However, intraperitoneally administered ginsenoside Rg5 nearly did not inhibit the PCA reaction. These ginsenosides not only suppressed the swelling of mouse ears induced by TPA, but also inhibited mRNA expression of cyclooxygenase-2, $TNF-{\alpha}$, and IL-4 and activation of transcription factor NF-kB. These inhibitions of ginsenoside Rh3 were more potent than those of ginsenoside Rg5. These findings suggest that ginsenoside Rg5 may be metabolized in vivo to ginsenoside Rh3 by human intestinal microflora, and ginsenoside Rh3 may improve antiallergic diseases, such as rhinitis and dermatitis.

• ALGAE
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• v.35 no.2
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• pp.201-212
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• 2020

The inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn disease are characterized by chronic inflammation throughout the gastrointestinal tract. The prevalence of IBD has been increasing worldwide, and has sometimes led to irreversible impairment of gastrointestinal structure and functions. In the present study, we identified a new sulfoquinovosylmonoacylglycerols (SQMG) (1) together with two known SQMGs (2 and 3) regulating intestinal inflammation from the brown alga Turbinaria ornata. The anti-inflammatory properties of two bioactive SQMGs, 1 and 2 were evaluated using an in vitro co-culture system consisting of human epithelial Caco-2 cells and PMA (phorbol 12-myristate 12-acetate)-differentiated THP-1 macrophages. Treatment with 1 or 2 inhibited the production nitric oxide and prostaglandin E₂ induced by lipopolysaccharide and interferon γ challenge. The expressions of inducible nitric oxide synthase and cyclooxygenase 2 were markedly down-regulated in response to inhibition of nuclear factor κB translocation to nucleus. These findings suggest the potential use of the brown alga T. ornata and its biologically active metabolites SQMGs as pharmaceutical adjuvants in the treatment of inflammation-related diseases, including IBD.

• Archives of Pharmacal Research
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• v.27 no.7
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• pp.683-692
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• 2004

Curcumin (diferuloylmethane) is a major naturally-occurring polyphenol of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. Curcumin has shown anti-carcinogenic activity in animal models. Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive oxygen-generating enzymes such as lipoxygenase/cyclooxygenase, xanthine dehydrogenase/oxidase and inducible nitric oxide synthase; and an effective inducer of heme oxygenase-1. Curcumin is also a potent inhibitor of protein kinase C(PKC), EGF(Epidermal growth factor)-receptor tyrosine kinase and LĸB kinase. Subsequently, curcumin inhibits the activation of NF(nucleor factor)KB and the expressions of oncogenes including c-jun, c-fos, c-myc, NIK, MAPKs, ERK, ELK, PI3K, Akt, CDKs and iNOS. It is proposed that curcumin may suppress tumor promotion through blocking signal transduction path-ways in the target cells. The oxidant tumor promoter TPA activates PKC by reacting with zinc thiolates present within the regulatory domain, while the oxidized form of cancer chemopreventive agent such as curcumin can inactivate PKC by oxidizing the vicinal thiols present within the catalytic domain. Recent studies indicated that proteasome-mediated degradation of cell proteins playa pivotal role in the regulation of several basic cellular processes including differentiation, proliferation, cell cycling, and apoptosis. It has been demonstrated that curcumin-induced apoptosis is mediated through the impairment of ubiquitin-proteasome pathway. Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin and that these compounds subsequently were converted to monoglucuronide conjugates. These results suggest that curcumin-glucuronide, dihydrocurcumin-glucuronide, tetrahydrocurcumin-glucuronide and tetrahydrocurcumin are the major metabolites of curcumin in mice, rats and humans.

• Proceedings of the SCSK Conference
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• 2003.09a
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• pp.601-610
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• 2003

Biotin is a water-soluble vitamin used as a skin conditioning agent and promotes the formation of intercellular lipid layers through increased lipid synthesis, which improves the skin's natural barrier function. The anti-inflammatory effects of biotin have been investigated using in vitro assay models, such as MTT assay, measurements of concentrations of nitric oxide(NO), prostaglandin E2(PGE$_2$), and inhibition rate of 5-lipoxygenase(5-LOX). In comparison with biotin, other plant extracts were tested at the same time which were kudzu vine extract, sage extract, paeonia extract, and dipotassium glycyrrhetinate. Nitric oxide is a signal molecule with functions such as neurotransmission, local vascular relaxation, and anti-inflammation in many physiological and pathological processes. NO can cause apoptosis and necrosis of target cells such as keratinocytes and is generated from L-arginine by nitric oxide synthase (NOS). Prostanoids, including prostaglandins and thromboxanes, are generated by the phospholipase $A_2$/cyclooxygenase(COX) pathway, and leukotrienes are generated by the 5-lipoxygenase pathway from arachidonic acid. Prostaglandin E2 recently have been shown to be beneficial in the resolution of tissue injury and inflammation, also has been implicated as an immunosuppressive agent and plasma levels of PGE$_2$ are elevated in patients sustaining thermal injury. Lipoxygenase metabolites from arachidonic acid have been implicated in inflammation, anti-inflammatory activity of the raw materials was evaluated in vitro by the offered inhibition of lipoxygenase.

• Tuberculosis and Respiratory Diseases
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• v.66 no.4
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• pp.274-279
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• 2009

Background: Uteroglobin (UG) is a secretary protein that has strong immunomodulatory properties, and which is synthesized in most epithelia including lung tissue. Overexpression of UG is associated with decreased expression of cyclooxygenase (COX)-2 and suppression of cancer cell growth. Indoleamine 2,3-dioxygenase (IDO) catalyzes tryptophan along the kynurenine pathway, and both the reduction in local tryptophan and the production of tryptophan metabolites contribute to the immunosuppressive effects of IDO. Methods: In this study, we investigated the pattern of expression of COX-2 and IDO, and the effect of UG transduction in the expression of COX-2 and IDO in several non-small cell lung cancer cell lines, especially A549. Results: Both COX-2 and IDO were constitutionally expressed in A549 and H460 cells, and was reduced by UG transduction. In A549 cells, the slightly increased expression of COX-2 and IDO with the instillation of interferon-gamma (IFN-$\gamma$) was reduced by UG transduction. However, the reduced expression of COX-2 and IDO by UG transduction was not increased with IFN-$\gamma$ instillation in A549 cells. In both the A549 COX-2 sense and the A549 COX-2 anti-sense small interfering RNA (siRNA)-transfected cells, IDO was expressed; expression was reduced by UG transduction, irrespective of the expression of COX-2. Conclusion: The results suggest that the anti-proliferative function of UG may be associated with the immune tolerance pathway of IDO, which is independent of the COX-2 pathway.