• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.27 no.3
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• pp.204-208
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• 2001

The purpose of this study is to examine the change of enzymeimmuno-assay for $prostaglandinE_2$ in the synovial fluid lavage specimen of patients with mandibular fracture patients without condylar fracture. For this study, fourteen patients (eight males, six females) with mandibular fractures without condylar fracture was investigated to analyse the synovial fluid from upper temporomandibular joint cavities. Synovial fluid was collected from TMJ cavities of mandibular fracture patients before open reduction and after one week of open reduction, and then stored in liquid nitrogen tank after centrifuge. Two synovial fluid lavage samples of TMJs of 2 asymptomatic served as normal controls referred from other data. The concentrations of $PGE_2$ were measured by use of $PGE_2$ EIA System ($Amersham^{(R)}$). The following results were obtained: 1) In nine patients, the concentrations of $PGE_2$ are lower after open reduction than before. 2) In three patients, the concentrations of $PGE_2$ are higher after open reduction than before. 3) There was no statistical significant between the preoperative group and postoperative 7 days (p>0.05), but there was some difference between the two groups. In conclusion, the results suggest that $PGE_2$ probably does not play as important role in the harm of TMJ.

• Journal of Veterinary Clinics
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• v.34 no.3
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• pp.172-177
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• 2017

Fucoidan, a cell wall polysaccharide found in the brown seaweed, is reported to have broad-spectrum biological activities. The objectives of this study were to examine the effect of fucoidan on prostaglandin $E_2$ ($PGE_2$) and cyclooxygenase-2 (COX-2) expression in lipopolysaccharide (LPS)-stimulated porcine peripheral blood mononuclear cells (PBMCs) and to determine whether these effects are involved in Akt activation. The levels of $PGE_2$ production in the culture supernatants from PBMCs were determined by the enzyme-linked immunosorbent assay (ELISA) kit and the levels of COX-2 mRNA were measured by real time polymerase chain reaction (RT-PCR). Akt activity was determined by Western blot analysis. Fucoidan in LPS-$na{\ddot{i}ve}$ PBMCs has no effect on $PGE_2$ production and COX-2 mRNA expression. Furthermore, fucoidan does not affect Akt activation in LPS- $na{\ddot{i}ve}$ PBMCs. However, $PGE_2$ production and COX-2 mRNA expression on PBMCs were remarkably enhanced by LPS stimulation. Akt activity was also increased by LPS. Increasing effects of $PGE_2$ production and COX-2 mRNA expression in PBMCs induced by LPS were suppressed by addition of fucoidan. In addition, fucoidan reduced an increase in Akt activity in LPS-stimulated PBMCs. These results suggested that fucoidan exerts potent anti-inflammatory properties by suppression of $PGE_2$ production, COX-2 mRNA expression and Akt activation in LPS-stimulated PBMCs.

• The Korean Journal of Physiology
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• v.14 no.2
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• pp.1-5
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• 1980

This study was undertaken to investigate the influence of prostaglandin $E_1(PGE_1)$ upon the activity of carbonic anhydrase and upon the inhibitory action of acetazolamide on carbonic anhydrase. The heparinized blood was sampled by cardiac puncture from Sprague-Dawley strain rats under ether anesthesia and was hemolysed by adding distilled water 1,000 times the amount of the blood. The activity of carbonic anhydrase of 0.1 ml of the hemolysate was measured by Maren's simplified micro-method. In the first experiment, the 7 rats were used, and the activity was measured by adding 0.1 ml of various concentrations of $PGE_1$(0.5, 1.25, 2.5, 5.0, 10 and $20\;{\mu}g/ml$). In the second experiment, the 6 rats were used and the activity was measured by adding 0.1 ml of $PGE_1(5\;{\mu}g/ml)$ and 0.1 ml of acetazolamide$(6{\times}10^{-7}M/l)$ respectively or simultaneously. Obtained results were as follows: 1) The activity of carbonic anhydrase was significantly inhibited by $PGE_1$ at doses of $0.5{\sim}10\;{\mu}g/ml$, maximally at a dose of $2.5\;{\mu}g/ml$, but inhibition was no more observed at a dose of $20\;{\mu}g/ml$. 2) The activity of the acetazolamide group was significantly less than that of the control group. 3) The activity of the $PGE_1+acetazolamide$ group was significantly less than those of the $PGE_1$ group and the acetazolamide group. It is inferred from the above results that the $PGE_1$ inhibits the activity of carbonic anhydrase dose-dependently and strengthens the inhibitory effect of acetazolamide on carbonic anhydrase.

• Journal of Pharmacopuncture
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• v.14 no.3
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• pp.81-90
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• 2011

Objectives : Angelicae Gigantis Radix has been known traditional medicine with antimicrobial activities and it has been widely used for treatment of blood and inflammatory diseases. In the present study, some studies examined anti-inflammation effects of Angelicae Gigantis Radix but they usually were performed by ethanol extracted Angelicae Gigantis Radix pharmacopuncture. So We investigated the inhibitory effects of Angelicae Gigantis Radix pharmacopuncture by hot water and ethanol extract on Nitric oxide(NO) and Prostaglandin $E_2$($PGE_2$) production in lipopolysaccharide(LPS) induced macrophage cell. Methods : Angelicae Gigantis Radix was extracted by ethanol and hot water. Cell viability was determined by MTT assay. To evaluate anti-inflammation effects of Angelicae Gigantis Radix pharmacopuncture, we examined NO and $PGE_2$ production in LPS induced macrophages. The concentrations of NO and $PGE_2$ were measured by Griess assay and Enzyme Immuno-Assay. Results : 1) The MTT assay demonstrated that cytotoxic effect of Angelicae Gigantis Radix pharmacopuncture by hot water extract and ethanol extract in RAW 264.7 macrophage cells were not appeared. 2) Angelicae Gigantis Radix pharmacopuncture by ethanol extract and hot water extract inhibited NO production in LPS induced macrophages significantly. 3) Angelicae Gigantis Radix pharmacopuncture by ethanol extract tended to inhibiting $PGE_2$ production in LPS induced macrophages. And Angelicae Gigantis Radix pharmacopuncture by hot water extract inhibited LPS induced production of $PGE_2$ in RAW 264.7 macrophage cells significantly. Conclusions : This study suggests that Angelicae Gigantis Radix pharmacopuncture may have an anti-inflammatory property through the inhibition of NO and $PGE_2$ production in LPS induced macrophages. It may have a therapeutic potential for the treatment of various inflammatory diseases.

• Restorative Dentistry and Endodontics
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• v.25 no.2
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• pp.193-201
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• 2000

Prostaglandins (PGs) and Leukotrienes (LTs) have been implicated in the genesis of pulpal and periapical inflammation. In this study, the relationships among $PGE_2$, 6-keto-PG $F_1{\alpha}$ (a stable metabolite of $PGI_2$) and $LTB_4$ concentrations in inflamed pulp and periapical lesions were discussed. Pulp tissue were obtained in routine endodontic treatment and periapical lesions in periapical surgery after clinical diagnoses were made. These specimens were divided into four groups as normal pulp group (Control group), acute pulpitis group, chronic pulpitis group, and periapical lesion group. Pulp tissue and periapical lesions were stored in liquid nitrogen. The concentration of $PGE_2$, $PGI_2$ and $LTB_4$ were measured with ELISA. The data were analyzed by one-way ANOVA. Significantly higher levels of $PGE_2$, 6-keto-PG $F_1{\alpha}$ a and $LTB_4$ were found in acute pulpitis group than chronic pulpitis group and periapical lesion group(p<0.05). Periapical lesion group showed significantly higher mean concentrations of $PGE_2$ and $LTB_4$ than chronic pulpitis group. In control and chronic pulpitis group, significant higher levels of $PGI_2$ than $PGE_2$ and $LTB_4$ were found. These results suggested that the high levels of $PGE_2$ and $LTB_4$ in periapical lesions may be due to rich endothelium., fibroblast and lymphocyte known as the main producers of $PGE_2$ and $LTB_4$. $PGI_2$ may be thought to one of the most abundant PGs in normal pulp tissue.

• Journal of dental hygiene science
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• v.15 no.6
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• pp.753-760
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• 2015

Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin $E_2(PGE_2)$ was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and $PGE_2$ and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and $PGE_2$ release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.50 no.1
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• pp.29-36
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• 2024

This study was carried out to identify the anti-inflammatory effects of Ishige foliacea (I. foliacea) extract on skin using RAW 264.7 cells. The anti-inflammatory effects of I. foliacea extract on RAW 264.7 cells were assessed by cell viability assay, mRNA expressions, and nitric oxide (NO)/prostaglandin E₂ (PGE₂) productions. The anti-inflammatory effects of I. foliacea extract were elucidated by analysis of IL-1α/IL-1β/IL-6/TNFα gene expressions and PGE₂/NO production. Quantitative real-time polymerase chain reaction showed that I. foliacea extract decreased the gene expression levels of iNOS/COX2/IL-1α/IL-1β and IL-6. Furthermore, PGE₂/NO production also revealed that I. foliacea extract exhibited anti-inflammatory properties. These results suggest that I. foliacea extract is an anti-inflammatory compound. It could be a potent cosmeceutical material for anti-inflammatory effects. Further studies on the anti-inflammatory mechanisms of broadleaf extracts are expected to help identify pharmacological mechanisms related to inflammation in addition to cosmeceuticals.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.

• Proceedings of the Materials Research Society of Korea Conference
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• 1999.05a
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• pp.142-142
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• 1999

• Journal of Life Science
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• v.19 no.10
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• pp.1396-1402
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• 2009

Hizikia fusiforme is a kind of edible brown seaweed that grows mainly in the northwest Pacific including Korea, Japan and China, and has been widely used as food in Korea. Induction of cyclooxygenase-2 (COX-2) expression and prostaglandin $E_2$ ($PGE_2$) production is thought to have beneficial immunomodulatory effects in acute and chronic inflammatory disorders. In this study, we investigated the effects of extracts of H. fusiforme on the expression of COX-2 and production of $PGE_2$ in U937 human pre-monocytic cell models. In U937 cells stimulated with phorbol 12-myristate 13-acetate (PMA) to mimic inflammation, methanol extract of H. fusiforme (MEHF) and ethanol extract of H. fusiforme (EEHF), but not water extract of H. fusiforme (WEHF), inhibited PMA-induced expression of both COX-2 protein and mRNA, which was associated with inhibition of $PGE_2$ production. To investigate the mechanism by which MEHF and EEHF inhibit COX-2 gene expression and $PGE_2$ production, we examined the activation of nuclear factor-kappaB (NF-$\kappa$B) in U937 cells. Pre-treatment with MEHF and EEHF significantly attenuated the PMA-induced IkappaB degradation and prevented nuclear translocation of NF-$\kappa$B. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-inflammatory activity of H. fusiforme.