• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.177-188
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• 1996

The effects of cytokines on the growth and differentiation of glial cells in culture were evaluated to confirm that cytokines could modify the number and function of glial cells. Proliferation of glial cells was determined by the $^3H-thymidine$ uptake and the double immunostain with anti-cell specific marker and anti-bromodeoxyuridine(BrdU) antibody. To check the effect on the differentiation of glial cells, the amount of glial fibrillar acidic protein(GFAP) and the activity of glutamine synthetase(GS) were measured in astrocytes. And also the amounts of myelin basic protein(MBP) and the activity of 2',3'-cyclic nucleotide phosphohydrolase(CNPase) were measured in oligodendrocytes. Among the cytokines used, only interleukin-$1{\beta}(IL-1{\beta})$ stimulated the growth of type 1 and type 2 astrocyte as well as 0-2A precursor cell. When the functional changes in these glial cells by cytokines were tested, $IL-1{\beta}$ did not increase GFAP content in type 1 and type 2 astrocyte, but $IL-1{\beta}$ increased GS activity in type 1 astrocyte, and slightly decreased this enzyme activity in type 2 astrocyte. Also interleukin-2(IL-2) and $interferon-{\gamma}$ $(IFN-{\gamma})$ inhibited the activity of GS in type 1 and type 2 astrocyte. On the other hand, all cytokines used did not modify the growth and differentiation in oligodendrocytes. From these results we could suggest that $IL-1{\beta}$ increases the growth of type 1 and type 2 astrocyte and also promotes the development for 0-2A precursor cell to type 2 astrocyte.

• Natural Product Sciences
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• v.21 no.4
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• pp.268-272
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• 2015

Sesquiterpene-quinone is a class of secondary metabolites frequently encountered from marine sponge. The present study was designed to examine the anti-inflammatory action of sponge-derived dactyloquinone B (DQB) and cyclospongiaquinone-1 (CSQ1) mixture using lipopolysaccharide (LPS)-induced inflammatory responses. We measured the production of nitric oxide (NO), tumor necrosis factor-alpha ($TNF-{\alpha}$), $interleukin-1{\beta}$ ($IL-1{\beta}$), and interleukin-6 (IL-6) and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein. $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 production, which increased by treatment with LPS, were significantly inhibited by DQB and CSQ1 mixture. It also decreased the production of NO production, and iNOS and COX-2 expression. Furthermore, it reduced 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ear edema of ICR mice. These results demonstrate that sesquiterpene-quinone, DQB and CSQ1 mixture, might serve as a chemical pipeline for the development of anti-inflammatory agent.

• Archives of Pharmacal Research
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• v.20 no.3
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• pp.234-238
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• 1997

CINC-1 is a member of chemokine family with chemotactic and activating properties to neutrophils. CINC-1 induction in IL-$1{\beta}$-stimulated rat fibroblast NRK-49F cells was quantitated by a sensitive ELISA. CINC-1 production was increased up to 135 ng/ml from basal 2-6 ng/ml by stimulation with IL-$1{\beta}$.Steroidal anti-inflammatory drugs including dexamethasone and prednisolone exhibited potent suppressive effects on IL-$1{\beta}$-induced CINC-1 production. Among 39 kinds of natural triterpenoids tested, acacigenin B exhibited the highest suppressive effects with about $10{\mu}M$ to be 50% of inhibition on the CINC-1 induction. The suppressive potency of acacigenin B on IL-$1{\beta}$induced CINC-1 production was about 10-fold less than that of the steroidal anti-inflammatory drugs.

• The Korean Journal of Mycology
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• v.46 no.2
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• pp.161-176
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• 2018

Fungal ${\beta}$-glucan, known to have immunostimulatory and antitumor activities, can be recognized by host immune cells as one of the pathogen-associated molecular patterns (PAMPs). Although there are several reports on the diverse immunostimulatory activities of ${\beta}$-glucan, little is known about the intracellular signal transduction of ${\beta}$-glucan. Stimulation of RAW264.7 macrophage cells with ${\beta}$-glucan from Ganoderma lucidum induced the expressions of dectin-1, toll-like receptor 2 (TLR2), TLR4, and TLR6 at the transcription stage. Treatment with ${\beta}$-glucan also induced inflammatory mediators such as macrophage inflammatory proteins (MIP)-$1{\alpha}$, MIP-$1{\beta}$, MIP-$1{\gamma}$, interleukin (IL)-$1{\beta}$, and tumor necrosis factor (TNF)-${\alpha}$. Treatment of the cells with polymyxin B, an inhibitor of lipopolysaccharides (LPS), blocked the induction of inflammatory mediators in LPS- or ${\beta}$-glucan-stimulated systems. Pretreatment of the cells in our cell culture system with LY294002, a phosphoinositide 3-kinase (PI3K) inhibitor, or U0126, a mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) kinase (MEK)1/MEK2 inhibitor, led to a reduction in the induction of inflammatory mediators in a concentration-dependent manner. These results show that stimulation of the macrophage cells by ${\beta}$-glucan induced the expressions of both dectin-1 and TLRs. We also found that the PI3K/Akt and MEK pathways were involved in the induction of inflammatory mediators in macrophage cells during intracellular signal transduction of ${\beta}$-glucan.

• Restorative Dentistry and Endodontics
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• v.32 no.3
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• pp.191-197
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• 2007

Mineral trioxide aggregate (MTA) would influence healing of periapical tissues by modulating the production of growth factors and cytokines from PDL fibroblasts, however, the studies are insufficient. Therefore, the purpose of this study was to monitor the expression of transforming growth factor-beta1 $(TGF-\beta1)$, fibroblast growth factor-2 (FGF-2), and interleukin-6 (IL-6) from PDL fibroblasts in the presence of MTA. The human PDL fibroblasts were seeded onto the set MTA or IRM at a level of $1\times10^5$ cells per unit well, and further incubated for 6, 12, 24, and 48 hours. The levels of $TGF-\beta1$, FGF-2 and IL-6 from the supernatant were measured by enzyme-linked immunosorbent assay (ELISA) The data were analyzed using one-way ANOVA. The level of $TGF-\beta1$ was down-reg ulated when the cells were grown in the presence of MTA except at 6 hours. The levels of FGF-2 release were significantly suppressed when PDL fibroblasts were grown in the presence of MTA or IRM at all time intervals (p < 0.05). The expressions of IL-6 from MTA treated co)Is were comparable to those of untreated control cells throughout the observation periods. We presume that this material inhibits the stimulatory function of growth factors on granulation tissue formation and in turn, it promotes the healing process modulated by other bone-remodeling cells.

• Nutrition Research and Practice
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• v.11 no.1
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• pp.43-50
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• 2017

BACKGROUND/OBJECTIVES: The present study investigated the hypothesis that a highly pure linear ${\beta}$-1,3-glucan produced by Agrobacterium sp. R259 enhances human natural killer (NK) cell activity and suppresses pro-inflammatory cytokines. SUBJECTS/METHODS: In an eight-week, double-blind, randomized, placebo-controlled clinical trial, 83 healthy adults with white blood cell counts of $4,000-8,000cells/{\mu}L$ were participated and randomly assigned to take two capsules per day containing either 350 mg ${\beta}$-1,3-glucan or placebo. Six participants withdrew their study consent or were excluded due to NK cell activity levels outside the normal range. NK cell activity and serum levels of immunoglobulin G (IgG) and cytokines, such as interferon (IFN)-${\gamma}$, interleukin (IL)-2, IL-4, IL-6, IL-10, IL-12 and tumor necrosis factor (TNF)-${\alpha}$ were measured. RESULTS: NK cell activity and the serum levels of IL-10 were significantly higher from baseline to week 8 in the ${\beta}$-glucan group compared with the placebo group (P = 0.048, P = 0.029). Consumption of ${\beta}$-1,3-glucan also significantly increased NK cell activity compared with placebo after adjusting for smoking and stress status (P = 0.009). In particular, the effect of ${\beta}$-1,3-glucan on NK cell activity was greater in participants with severe stress than in those experiencing mild stress. However, the administration ${\beta}$-1,3-glucan did not significantly modulate the levels of IFN-${\gamma}$, IL-2, IL-4, IL-6, IL-12, TNF-${\alpha}$ and IgG compared with the placebo. CONCLUSION: The results showed that supplementation with bacterial ${\beta}$-1,3-glucan significantly increased NK cell activity without causing any adverse effects. Additionally, the beneficial effect of ${\beta}$-1,3-glucan on NK cell activity was greater in participants experiencing severe stress.

• Journal of the Korean Society of Radiology
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• v.13 no.1
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• pp.133-140
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• 2019

Triglycerides (TG) are one of the triggers of chronic inflammatory lesions in the blood vessels. In the key factors in the development of inflammatory diseases, Pro-inflammatory cytokines such as tumor necrosis factor-alpha $(TNF-){\alpha}$ and interleukin-1 beta ($IL-1{\beta}$) contribute to the development of inflammatory lesions by recruiting other immune cells in the inflamed area or causing cell necrotic death. In this study, I investigated the effect of Jurkat T lymphocytes and U937 monocytes involved in vascular inflammation development on the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ on exposure to TGs. In Jurkat cells, mRNA expression of $TNF-{\alpha}$ is increased by exposure to TGs. However, the expression levels of $TNF-{\alpha}$ and $IL-1{\beta}$ were increased by TGs in U937 cells. To investigate whether inducible nitric oxide synthase (iNOS) is involved in the increase of expression of $TNF-{\alpha}$ and $IL-1{\beta}$ by TGs, treatment of W1400 (an iNOS inhibitor) resulted in recovery of expression level both $TNF-{\alpha}$ and $IL-1{\beta}$. Based on the present study, it was confirmed that the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ in monocytes and T lymphocytes. This increased cytokines contribute to development of vascular inflammatory lesions. In addition, iNOS is involved in the increase of $TNF-{\alpha}$ and $IL-1{\beta}$ expression by TGs.

• The Journal of Korean Medicine
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• v.30 no.6
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• pp.35-43
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• 2009

Objectives: Hwangryunhaedok-tang (HRHDT), a prescription composed of four herbs, has been wi dely used in Oriental Medicine for the treatment of cerebral infarction. However, the mechanisms by which the herbal formula affects on the production of pro- and anti-inflammatory cytokines in cerebral infarction patients remain unknown yet. Methods: The levels of pro- and anti-inflammatory cytokines, including tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and IL-6, IL-10, and TGF-${\beta}1$ were determined in peripheral blood mononuclear cells (PBMCs) from cerebral infarction patients under our experimental conditions. Results: The secretory levels of pro- and anti-inflammatory cytokines, including tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and IL-6, and IL-10 were significantly increased in phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMCs) from cerebral infarction patients. However, pretreatment with HRHDT significantly inhibited the secretion of pro- and anti-inflammatory in PBMCs. Also, HRHDT induced a significant increase of transforming growth factor (TGF)-b1 in PBMCs. Conclusions: These data indicate that HRHDT may be beneficial in the suppression of inflammatory processes of cerebral infarct through suppression of TNF-$\alpha$, IL-$1{\beta}$, IL-6, and IL-10 and induction of TGF-${\beta}1$.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.89-94
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• 2004

The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 $(0.1,\;1,\;10,\;20\;ng/2\;{\mu}l)$ or Ang II $(600\;ng/10\;{\mu}l)$. A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. $IL-1\;{\beta}$ increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. $IL-1\;{\beta}$. Both i.c.v. $IL-1\;{\alpha}\;and\;{\beta}$ produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of $IL-1\;{\beta}$, the magnitude of MAP fall was not different from the control. The $IL-1\;{\beta}$ group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.

• Journal of Pharmacopuncture
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• v.4 no.1
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• pp.5-21
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• 2001

The influence of electroacupuncture (EA), a traditional Chinese medical treatment, on type Ⅱ collagen-induced arthritis (CIA) was examined in DBA/1J mice in vivo. Mice were immunized intradermally twice at the 3-week interval with bovine type Ⅱ collagen(C Ⅱ). EA stimulation, begun on the 21 simultaneously with the second immunization, was applied at the acupoint equivalent to GV4 three times a week for 3 weeks. The results showed that EA delayed the onset, attenuated the severity of arthritis, and reduced the anti-collagen antibody level. Furthermore, we investigated the impact of EA on the productions of endogenous $interleukin-1{\Beta}$ (IL-1 beta) and prostaglandin E2 (PGE2), and the levels of IL-1 beta mRNA in splenocytes and synovial tissues from C Ⅱ immunized mice on the 45 and cyclooxygenase-2 (COX-2) mRNA in lipopolysaccharide (LPS)-stimulated macrophages of normal mice by using reverse transcriptase-polymerase chain reaction (RT-PCR). EA stimulation significant inhibited the concentrations of splenic endogenous IL-1 beta and serum PGE2. The expression of IL-1 beta mRNA in spleen cells was obviously down-regulated and that in synovial tissues was modestly affected by EA. COX-2 mRNA was highly expressed in cultured peritoneal macrophages when stimulated with LPS. Previous treatment with EA also reduced LPS-stimulated induction of COX-2 mRNA. These data suggest that EA has an inhibitory effect on murine CIA, and the partial mechanism of its therapeutic result may be attributed to inhibiting the productions of IL-1 beta and PGE2 by suppression the IL-1 beta and COX-2 gene activations.