• Title/Summary/Keyword: prostaglandin E2 (PGE2)

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Role of Alveolar Macrophages in Productions of Prostaglandin D2 and E2 in the Inflamed Lung (프로스타글란딘 D2와 E2의 생성에 대한 허파 마크로파이지의 역할)

  • Joo, Myung-Soo
    • Journal of Life Science
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    • v.20 no.6
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    • pp.845-852
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    • 2010
  • Our previous study showed that lungs infected by Pseudomonas, a gram-negative bacteria, produce prostaglandin $D_2$ ($PGD_2$) and prostaglandin $E_2$ ($PGE_2$), the two major prostanoids generated by cyclooxygenase-2 (COX-2), and that the ratio of $PGD_2$ and $PGE_2$ can affect the outcome of the bacterial lung infection. In this study, we sought to uncover the mechanism that determines the ratio of $PGD_2$ and $PGE_2$ produced in lung inflammation. When treated with lipopolysaccharide (LPS), primary alveolar macrophages, extracted from mouse lung, more $PGE_2$ was produced than $PGD_2$, whereas MH-S, a murine alveolar macrophage cell line, produced more $PGD_2$ than $PGE_2$ in a similar experiment. Western blot analyses showed that the kinetics of COX-2 expression in both cell types is similar and epigenetic silencing of COX-2 expression did not affect expressions of lipocalin-PGD synthase (L-PGDS) and PGE synthase (mPGES-1), major enzymes synthesizing $PGD_2$ and $PGE_2$ in inflammation, respectively, indicating no effect of COX-2 on expressions of the two enzymes. Expressions of L-PGDS and mPGES-1 were also similar in both cell types, suggesting no effect of the two key enzymes in determining the ratio of $PGD_2$ and $PGE_2$ in these cells. A single intraperitoneal injection of LPS to C57BL/6 mice induced COX-2 expression and, similar to alveolar macrophages, produced more $PGE_2$ than $PGD_2$ in the lung. These results suggest that the differential expressions of $PGD_2$ and $PGE_2$ in the lung reflect those in alveolar macrophages and may not be directly determined by the enzymes responsible for $PGD_2$ and $PGE_2$ synthesis.

Diphlorethohydroxycarmalol, Isolated from Ishige okamurae, Increases Prostaglandin E2 through the Expression of Cyclooxygenase-1 and -2 in HaCaT Human Keratinocytes

  • Kang, Gyeoung-Jin;Han, Sang-Chul;Koh, Young-Sang;Kang, Hee-Kyoung;Jeon, You-Jin;Yoo, Eun-Sook
    • Biomolecules & Therapeutics
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    • v.20 no.6
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    • pp.520-525
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    • 2012
  • Prostaglandin (PG) $E_2$, the most abundant prostaglandin in the human body, is synthesized from arachidonic acid via the actions of cyclooxygenase (COX) enzymes. $PGE_2$ exerts homeostatic, cytoprotective, inflammatory, and in some cases anti-inflammatory effects. Also, it has been reported that $PGE_2$ is involved in hair growth. Diphlorethohydroxycarmalol (DPHC) is a phlorotannin compound isolated from the brown algae Ishige okamurae, with various biological activities in vitro and in vivo. In this study, the biological effect and mechanism of action of DPHC on prostaglandin synthesis in HaCaT human keratinocytes was examined. The results showed that, in these cells, DPHC significantly and dose-dependently induced $PGE_2$ synthesis by increasing the protein and mRNA levels of COX-1 and COX-2. Interestingly, DPHC-induced COX-1 expression preceded that of COX-2. Also, while both rofecoxib and indomethacin inhibited $PGE_2$ production, the latter was seems to be the more potent. From above results, we can expect that DPHC has some beneficial effects via increasing of $PGE_2$ production.

Suppression of Prostaglandin E2-Mediated Cell Proliferation and Signal Transduction by Resveratrol in Human Colon Cancer Cells

  • Song, Su-Hyun;Min, Hye-Young;Lee, Sang-Kook
    • Biomolecules & Therapeutics
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    • v.18 no.4
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    • pp.402-410
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    • 2010
  • Although the overproduction of prostaglandin $E_2$ ($PGE_2$) in intestinal epithelial cells has been considered to be highly correlated with the colorectal carcinogenesis, the precise mechanism of action remains poorly elucidated. Accumulating evidence suggests that the PGE receptor (EP)-mediated signal transduction pathway might play an important role in this process. In the present study, we investigated the mechanism of action underlying $PGE_2$-mediated cell proliferation and the effect of resveratrol on the proliferation of human colon cancer cells in terms of the modulating $PGE_2$-mediated signaling pathway. $PGE_2$ stimulated the proliferation of several human colon cancer cells and activated growth-stimulatory signal transduction, including Akt and ERK. $PGE_2$ also increased the phosphorylation of GSK-$3{\beta}$, the translocation of ${\beta}$-catenin into the nucleus, and the expressions of c-myc and cyclin D1. Resveratrol, a cancer chemopreventive phytochemical, however, inhibited $PGE_2$-induced growth stimulation and also suppressed $PGE_2$-mediated signal transduction, as well as ${\beta}$-catenin/T cell factor-mediated transcription in human colon cancer cells. These findings present an additional mechanism through which resveratrol affects the regulation of human colon cancer cell growth.

Effects of Ethanol Extract from Lathyrus palustris on Anti-inflammation Response of RAW 264.7 Cell (RAW 264.7 대식세포 염증반응에 대한 털연리초 에탄올 추출물의 항염증 효과)

  • Nam, Jung Hwan
    • Korean Journal of Plant Resources
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    • v.33 no.4
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    • pp.287-292
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    • 2020
  • Lathyrus palustris often used as a treatment for inflammation of the kidneys in Korean traditional medication. Generally, drugs for arthritis have anti-inflammatory and antinociceptive properties. However, the validity of the anti-inflammatory effect has not been scientifically investigated so far. Therefore, the purpose of the research was to investigate the latent anti-inflammatory ability of L. palustris using the ethanol extract. To evaluate the anti-inflammatory activities, we examined the inflammatory arbitrators such as a nitric oxide (NO) and prostaglandin E2 (PGE2) on RAW 264.7 cells. Our results indicated that ethanol extract significantly inhibited the lipopolysaccharide E (LPS) derived PGE2 production in RAW 264.7 cell. The inhibitory activity of ethanol extract for PGE2 tests with inhibition ratio showed in 40 ㎍/mL. Overall, PGE2 tests had a higher inhibitory effect on inflammation than NO tests. This result anticipated that the ethanol extract from L. palustris is a good candidate for developing the origin of anti-inflammatory agents.

Morphologic Study of Effects of Prostaglandin E2 and Evening Primrose Oil on Early Orthodontic Tooth Movement in Rats (백서의 구치 이동 초기에 Prostaglandin E2와 Evening Primrose Oil의 영향에 관한 형태학적 연구)

  • Lee, Won-Yu
    • The korean journal of orthodontics
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    • v.20 no.1
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    • pp.61-86
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    • 1990
  • To study the effect of prostglandin $E_2$ and evening primrose oil on orthodontic tooth movement in rats, one hundred and sixty rats were divided into four groups of 40 rats each. One group, injected with saline on the palate subperiosteally, served as a control group. A second and third group were injected subperiosteally on the palate with $PGE_2$ $10{\mu}g$ and evening primrose oil 10mg respectively. The fourth group was given indomethacin $20{\mu}g/m{\ell}$ orally by water bottle. The maxillary first molar was moved mesially from the incisors using a 50gm force rubber band. In each group at the 1, 2, 3, 5, and 7th day, 4 rats were examined by light microscope, and 4 by electron microscope. The obtained results were as follows: 1. Osteoclastic activity was maximum at the 3rd day in the $PGE_2$ group on the interradicular alveolar bone of the first molar, followed by the evening primrose oil group, control group, and indomethacin group. 2. Root resorption and vacuolar changes were maximum in the $PGE_2$ group. 3. At the 3rd day of the $PGE_2$ group, the osteoclasts showed well developed ruffled borders and clear zones. At the same day, the evening primrose oil group also showed well developed ruffled borders and clear zones, but less than the $PGE_2$ group. 4. At the 3rd and 5th day of the $PGE_2$ group, fibroblasts showed phagocytized fragmented collagen fibers in the cytoplasm. At the 7th day of the $PGE_2$ group, fibroblasts showed collagen fibers forming at the cell membrane surface.

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Induction of Prostaglandin E2 by Porphyromonas gingivalis in Human Dental Pulp Cells

  • Kim, So-Hee;Paek, Yun-Woong;Kang, In-Chol
    • International Journal of Oral Biology
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    • v.42 no.4
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    • pp.149-153
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    • 2017
  • Cyclooxygenase-2 (COX-2)-mediated prostaglandin $E_2$ ($PGE_2$) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and $PGE_2$ by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of $PGE_2$ were released from P. gingivalis-infected HDPCs and this $PGE_2$ increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) was demonstrated by the results of phosphorylation of $NF-{\kappa}B$ p65 and degradation of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$). Pharmacological inhibition of each of the three types of MAPKs and $NF-{\kappa}B$ substantially attenuated P. gingivalis-induced $PGE_2$ production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce $PGE_2$.

Effect of Sanyeoleumja on Inflammatory Response of RAW 264.7 Cells (RAW 264.7 cell의 염증반응에 대한 산열음자(散熱飮子)의 항염증 효과)

  • Kim, Tae Yeon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.34 no.1
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    • pp.7-13
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    • 2020
  • Sanyeoleumja (SY) is the traditional Korean medicinal prescription for the treatment of inflammatory diseases of eyes. In this study, the anti-inflammatory effects of SY water extract were investigated. To measure the anti-inflammatory effects of SY, we examined the productions of inflammatory factor including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), interleukin-1β (IL-1β) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. SY inhibited NO and PGE2 production in a dose dependent manner and decreased the protein and mRNA expression of iNOS and COX-2. Also, SY decreased the mRNA expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β). In conclusion, SY downregulated LPS-induced inflammatory factor productions, which could be a clinical basis for inflammatory diseases.

Hizikia fusiforme Inhibits Cyclooxygenase-2 Expression and Prostaglandin E2 Production by PMA through Inactivation of NF-κB (PMA에 의한 cyclooxygenase-2 발현 및 prostaglandin E2의 생성 증가에 미치는 톳 추출물의 영향)

  • Park, Cheol;Choi, Yung-Hyun
    • 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.

Anti-inflammatory Effect of the Processed Gardeniae Fructus in LPS-induced Macrophages (LPS로 유도된 대식세포에서 수치 치자의 항염효과)

  • An, Iseul;Kim, Sang Chan;Byun, Sung Hui;Lee, Jong Rok;Park, Sook Jahr
    • Herbal Formula Science
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    • v.27 no.4
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    • pp.245-255
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    • 2019
  • Objective : Herbal processing is one of the traditional techniques used in Korean medicine to increase the effectiveness of herbs or reduce their toxicity. In this study, Gardeniae Fructus processed with ginger juice and alcohol was prepared to evaluate the anti-inflammatory effect on lipopolysaccharide (LPS)-induced macrophages. Methods : The processing of Gardeniae Fructus was performed by adding 40 % ginger juice or 10% alcohol to the total weight of Gardeniae Fructus and then roasting at 150℃ for 5 minutes. Cell viability was determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To detect nitric oxide (NO) production, culture media were mixed with Griess reagent and measured the absorbance at 540 nm. Prostaglandin E2 (PGE2) and pro-inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was applied to monitor protein expression levels. Results : LPS-induced NO, PGE2 and inflammatory cytokines were decreased by the treatment of normal or processed Gardeniae Fructus ethanol extracts (GFE). Compared to normal GFE, the processed GFE showed a stronger inhibitory effect on the production of NO and PGE2. These inhibitory effect of GFE was due to the suppression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mediated from the inhibition of nuclear factor kappa B (NF-κB). Furthermore, processed GFE showed more suppressive effects on the expression of iNOS, COX-2 and IκBα proteins than normal GFE. Conclusion : From these results, it was concluded that GFE had an improved anti-inflammatory effect compared to normal GFE. These results provide an objective evidences for the use of herbal processing in Korean medicine.

Prostaglandin E2 Reverses Curcumin-Induced Inhibition of Survival Signal Pathways in Human Colorectal Carcinoma (HCT-15) Cell Lines

  • Shehzad, Adeeb;Islam, Salman Ul;Lee, Jaetae;Lee, Young Sup
    • Molecules and Cells
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    • v.37 no.12
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    • pp.899-906
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    • 2014
  • Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.