• Journal of Animal Science and Technology
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• v.53 no.3
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• pp.203-209
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• 2011

Lysophosphatidic acid (LPA) is a small lipid molecule that plays an important role through LPA receptors (LPARs) in reproductive processes. Our previous study has shown maximal expression of LPAR3 in the uterine endometrium on day (D) 12 of pregnancy in pigs, the period when conceptus secretes various molecules such as estrogen and interleukin-$1{\beta}$ (IL1B) and initiates implantation. We determined that endometrial expression of LPAR3 was increased by conceptus estrogen in the previous study, but the effect of IL1B on LPAR3 expression has not been determined. Thus, in this study we examined whether LPAR3 expression was also affected by IL1B. Endometrial explant cultures from D12 of the estrous cycle showed that levels of endometrial LPAR3 expression did not changed in response to IL1B. We also investigated LPAR3 expression in the uterine endometrium on D12 and D30 of pregnancy from gilts with conceptuses derived from somatic cell nuclear transfer (SCNT). The expression of LPAR3 mRNA was lower in endometria from gilts with conceptuses resulting from SCNT compared with those from gilts with embryos resulting from natural mating on D12 of pregnancy, but it was not different between them on D30 of pregnancy. Our results indicate that estrogen of conceptus origin is responsible for induction of LPAR3 expression during the peri-implantation period and appropriate LPA signaling is impaired in the uterine endometrium with SCNT-derived conceptuses during the implantation period in pigs.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.5
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• pp.370-378
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• 2005

The purpose of this study is that evaluate the distribution and biological roles of TNF-a, interleukin-1${\beta}$(IL-1${\beta}$), interleukin-6(IL-6) and tissue inhibitors of metalloproteinase-1(TIMP-1) in the synovial fliud of patients with non-inflammatory chronic temporomandibular joint(TMJ) disorders in relation to pain during joint movements and magnetic resonance imaging(MRI) findings. TMJ synovial fluids aspirates were obtained from 36 patients (36 joints) with chronic TMJ disorders and from 8 controls(8 joints). Patients were divided to four groups. The control group was from healthy volunteers(8 joints), group I(18 joints) was patients with anterior disc displacement with reduction, group II(5 joints) was patients with disc displacement without reduction and group III (5 joints) was osteoarthritis. The TNF-${\alpha}$, IL-1${\beta}$ and IL-6 levels in the aspirates were determined by using an enzyme-linked immunosorbent assay and the TIMP-1 level was measured by an enzyme immunoassay. Following examinations for pain during joint movements and MRI observations, these cytokines' level and frequencies of detection were compared. The level of IL-1${\beta}$was not significant different in all groups. but the level of TNF-${\alpha}$, IL-6 and TIMP-1 were significant different among groups. The level of IL-6 and TIMP-1 were correlated to pain during movement(p<0.01) and the level of TNF-a(p<0.05). Also, the level of IL-6 was correlated to the level of TIMP-1(p<0.01). Especially, The level of the TIMP-1 level was significantly correlated to the pain during movement and showed very high levle of Pearson's correlation coefficient (r=0.833)(p<0.001). The results indicated that the TNF-${\alpha}$, IL-6 and TIMP-1 levels in the TMJ aspirates of patients with chronic TMJ disorders have been raised. Especially, IL-6 and TIMP-1 were very high levels in the patients who were degraded in the TMJ. Also, TNF-${\alpha}$, IL-6 and TIMP-1 showed the significant correlation in the chronic temporomandibular joint disorders. Therefore I suggest that these cytokines were also correlated to the pain during movement in the chronic temporomandibular joint disorders.

• 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.

• Journal of Marine Bioscience and Biotechnology
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• v.12 no.2
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• pp.99-107
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• 2020

Osteoarthritis (OA) is an inflammatory degenerative joint disease that is accompanied by irreversible joint cartilage destruction. Recently, the antioxidant effects of Carpomitra costata, which is a type of brown algae, have been reported, but their effects on OA have not been investigated. In this study, the anti-osteoarthritic effect of the ethanol extract of C. costata (EECC) on SW1353 human chondrocytes was studied. Results showed that EECC significantly attenuated the interleukin-1β (IL-1β)-induced release of pro-inflammatory mediators, including prostaglandin E2 and nitric oxide (NO), as well as expressions of cyclo-oxygenase-2 and inducible NO synthase. EECC also inhibited the IL-1β-induced expressions of matrix metalloproteinase-1, -3, and -13 in SW1353 chondrocytes, which reduced their extracellular secretion. In addition, the oxidative stress induced by IL-1β was confirmed to be blocked by EECC due to the inhibition of reactive oxygen species generation. Moreover, EECC suppressed IL-1β-mediated translocation of nuclear factor-kappa B (NF-κB) from cytosol into the nucleus and the degradation of IκB-α, which indicates that EECC exhibits anti-inflammatory effects by inhibiting the NF-κB signaling pathway. These results are the first to demonstrate the anti-inflammatory activities of C. costata extracts in chondrocytes, thus suggesting that this algae extract may be used in the treatment of OA.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.1
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• pp.204-211
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• 2005

We hypothesize that bear's gall may have a certain role in anti-inflammation through a preventive effect of pro-inflammatory potentials. Secondly, we tried to connect the experimental results to Alzheimer's disease (AD), which chronic inflammation is a main cause of the disease. For this theme, we designed to elucidate the efficacy of bear's gall in suppressing the pro-inflammatory mediators, such as nitric oxide (NO) and $interleukin-1{\beta}\;(IL-1{\beta})$ in rat microglia. From the study, we concluded that bear's gall plays a positive role in suppressing such pro-inflammatory repertoire from rat microglia comparing to normal and positive control, such as culture media and cyclosporine. Interestingly, bear's gall showed a prolonged effect of anti-inflammation comparing with cyclosporine when time goes by up to 48h with a significant suppression at $1.2\;mg/m{\ell}$. Therefore, we can consider that bear's gall in part can be applied to AD therapy in that it suppresses the expression of pro-inflammatory mediators as well as its continued effect.

• Molecular & Cellular Toxicology
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• v.1 no.1
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• pp.40-45
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• 2005

Ursodeoxycholic acid (UDCA) has long been used as an adjuvant or first choice of therapy for liver disease. Commonly, UDCA has been reported to play a role in improving hyperbilirubinemia and disorder of bromsulphalein. More commonly, UDCA has been used in reducing the rate of cholesterol level in bile juice that can cause cholesterol stone. The effects on the promotion of bile acid release that leads an excretion of toxic materials and wastes produced in liver cells as well as various arrays of liver disease such as hepatitis. Other than already reported in clinical use, immunosuppressive effect has been studied, especially in transplantation. In the study, we hypothesized that UDCA might have a certain role in anti-inflammation through a preventive effect of pro-inflammatory potentials in the brain macrophages, microglia. We found that the treatment of $200\;{\mu}g/ml$ UDCA effectively suppressed the pro-inflammatory mediators (i.e. nitric oxide and interleukin-$1{\beta}$) in rat microglia compared to comparators. Interestingly, RT-PCR analysis suggested that UDCA strongly attenuated the expression of $IL-1{\beta}$ that was comparable with cyclosporine A at 48 h incubation. Conclusively, we found that UDCA may playa cytoprotective role in microglial cells through direct or indirect pathways by scavenging a toxic compound or an anti-inflammatory effect, which are known as major causes of neurodegenerative diseases.

• Journal of Nutrition and Health
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• v.49 no.4
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• pp.241-246
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• 2016

Purpose: Aloe-emodin (AE), an ingredient of aloe, is known to exhibit anti-inflammatory activities. However, little is known about the underlying molecular mechanisms of its inflammatory modulatory activity in vitro. In the present study, we investigated the anti-inflammatory potential of AE using $Pam_3CSK_4$-stimulated macrophages. Methods: RAW 264.7 macrophages were treated with AE (0~20 mM) for 1 h, followed by treatment with $Pam_3CSK_4$ for 1 h. After incubation, mRNA expression levels of cytokines were measured. The effect of AE on TLR2-related molecules was also investigated in $Pam_3CSK_4$-stimulated RAW 264.7 macrophages. Results: AE attenuated $Pam_3CSK_4$-stimulated expression of proinflammatory cytokines, including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-6 (IL-6), and interleukin-$1{\beta}$ ($IL-1{\beta}$) in RAW 264.7 macrophages. Two concentrations of AE ($10{\mu}M$ and $20{\mu}M$) effectively reduced mRNA expression of TLR2 by 41.18% and 54.43%, respectively, compared to that in control cells (p < 0.05). AE also decreased nuclear factor-kappa B ($NF-{\kappa}B$) activation and mitogen-activated protein kinase (MAPK) phosphorylation. Phosphorylation levels of ERK1/2, p38, and JNK were markedly reduced by $20{\mu}M$ AE. In particular, AE decreased phosphorylation of ERK in a dose-dependent manner in $Pam_3CSK_4$-stimulated RAW 264.7 macrophages. Conclusion: Our data indicate that AE exerts its anti-inflammatory effect by suppressing TLR2-mediated activation of $NF-{\kappa}B$ and MAPK signaling pathways in macrophages.

• Archives of Pharmacal Research
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• v.29 no.8
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• pp.685-690
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• 2006

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite ginsenoside Rh3 in a chronic dermatitis model was investigated. Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin $(IL)-1{\beta}$, tumor necrosis factor $(TNF)-{\alpha}$ and interferon $(IFN)-{\gamma}$. The inhibition of ginsenoside Rh3 was more potent than that of ginsenoside Rg5. These findings suggest that ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of $IL-1{\beta}$ and $TNF-{\alpha}$ produced by macrophage cells and of $IFN-{\gamma}$ produced by Th cells.

• Herbal Formula Science
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• v.18 no.1
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• pp.121-132
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• 2010

Inflammatory reaction is characterized by over-production of inflammatory mediators due to an up-regulation of inflammatory pathways, which produce pro-inflammatory mediators, such as interleukin-1beta (IL-$1{\beta}$), IL-6, tumour necrosis factor alpha (TNF-$\alpha$), prostaglantin $E_2$ ($PGE_2$), and nitric oxide (NO) in U937 cells. We investigate the anti-inflammatory effects of water extracts from Lonicerae Flos and Scutellariae Radix in lipopolysaccharide (LPS)-stimulated U937 cells. Each extract suppressed the production of inflammatory mediators (NO, IL-$1{\beta}$, TNF-$\alpha$, and $PGE_2$) and the expression of inducible NO synthase and cyclooxygenase-2 in LPS- stimulated U937 cells in a dose-dependent manner. These suppressive effects were synergistically increased by their combination. Their combination extract also inhibited NF-${\kappa}B$-DNA complex of NF-${\kappa}B$ binding activity and translocation of NF-${\kappa}B$ from cytosol to nucleus. These results suggest that the combination of water-extractable components of Lonicerae Flos and Scutellariae Radix may be useful for therapeutic drugs against inflammatory immune diseases, probably by suppressing the production of inflammatory mediators.

• Molecular & Cellular Toxicology
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• v.5 no.1
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• pp.44-50
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• 2009

This study was conducted to evaluate the inflammation mechanisms of tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-4 (IL-4), and IL-$1{\beta}$-induced stimulation of A549 human epithelial cells. In the present study, A549 cells were stimulated with TNF-$\alpha$, IL-4 and IL-$1{\beta}$ to induce expression of chemokines and adhesion molecules involved in eosinophil chemotaxis. The effects of TNF-$\alpha$, IL-4 and IL-$1{\beta}$ on gene expression profiles in A549 cells were evaluated by oligonucleotide microarray and Real time RT-PCR. The gene expression profiles for the A549 cells varied depending on the cytokines. Also, the results of the microarray and Real time RT-PCR revealed that inflammatory-related genes were up-regulated in cytokine stimulated A549 cells. Cytokines can affect inflammation in A549 cells. A microarray-based genomic survey is a high-throughput approach that enables evaluation of gene expression in cytokine stimulated cell lines.