• 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.

• Intestinal research
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• v.15 no.1
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• pp.75-82
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• 2017

Background/Aims: Cyclooxygenase-2 (COX-2), 15-hydroxyprostaglandin dehydrogenase (15-PGDH), and microsomal prostaglandin E synthase-1 (mPGEs-1) regulate prostaglandin $E_2$ ($PGE_2$) expression and are involved in colon carcinogenesis. We investigated the expression of $PGE_2$ and its regulating genes in sporadic human colon tumors and matched normal tissues. Methods: Twenty colonic adenomas and 27 colonic adenocarcinomas were evaluated. COX-2 and 15-PGDH expression was quantified by real-time polymerase chain reaction. The expression of $PGE_2$ and mPGEs-1 was measured using enzyme-linked immunosorbent assay and Western blotting, respectively. Results: The expression of COX-2, mPGEs-1, and $PGE_2$ did not differ between the adenomas and matched distant normal tissues. 15-PGDH expression was lower in adenomas than in the matched normal colonic tissues (P<0.001). In adenocarcinomas, mPGEs-1 and $PGE_2$ expression was significantly higher (P<0.001 and P=0.020, respectively), and COX-2 expression did not differ from that in normal tissues (P=0.207). 15-PGDH expression was significantly lower in the normal colonic mucosa from adenocarcinoma patients than in the normal mucosa from adenoma patients (P=0.018). Conclusions: Early inactivation of 15-PGDH, followed by activation of COX-2 and mPGEs-1, contributes to $PGE_2$ production, leading to colon carcinogenesis. 15-PGDH might be a novel candidate marker for early detection of field defects in colon carcinogenesis.

• 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.

• Archives of Plastic Surgery
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• v.32 no.1
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• pp.5-11
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• 2005

Prostaglandin $E_1$($PGE_1$) is known to have various physiological action such as vasodilatation, decrease of blood pressure, angiogenesis, inhibition of platelet aggregation and so forth. $PGE_1$ has been developed in many different formulations in order to overcome its chemical instability and deactivation in the lungs when administered parenterally. Lipo-AS013 is a potent drug with higher chemical stability and greater vascular wall targeting than others. The study was done on $3{\times}10cm$ model flap of dorsal skin of Sprague-Dawley rats and the flap perfusion survival were observed and documented. The flap treated with Lipo-AS013 beforehand was given intravenously Sodium fluorescein 10 minutes later, and then Percent Dye Fluorescence Index(% DFI) was calculated. The results were compared to a control group and the group administered locally epinephrine.. In the control group, the % DFI and flap survival rate increased from $54.1{\pm}6.7$ to $65.0{\pm}2.6$(p<0.01) while in Lipo-AS013 group from $55.3{\pm}2.2$ to $67.4{\pm}1.9$(p<0.01), respectively. In the epinephrine group, the % DFI(p<0.05) and flap survival rate(p<0.001) decreased. In the both epinephrine and Lipo-AS013 group Percent DFI and flap survival rate are comparable with the control group.The result indicates that the potent Lipo-AS013 enhances the blood flow and flap survival. This highly potent Lipo-AS013 may have targeting ability and accumulate $PGE_1$ onto the vascular walls. A quantitative analysis of fluorescence on the skin surface is a reliable tool to measure the blood perfusion into an ischemic flap and its viability. Further comparative study with conventional $PGE_1$ and Lipo-$PGE_1$ is needed in order to clarify the action and efficiency of Lipo-AS013.

• The Korean Journal of Pain
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• v.20 no.1
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• pp.15-20
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• 2007

Background: Lipo-prostaglandin E1 (Lipo-$PGE_1$) has vasodilating and platelet aggregation inhibitory characteristics and it has been used as a treatment for patients with blood flow dysfunction disease. Based on the mechanisms of lumbar spinal stenosis, including veno congestion, neuro-ischemia and mechanical compression, we aimed to study whether intravenous Lipo-$PGE_1$ injection has any therapeutic effect on hyperalgesia in a rat foraminal stenosis model. Methods: In this study, twenty male Sprague-Dawley rats were divided into the control (n = 10) and Lipo-$PGE_1$ (n = 10) groups. A small stainless steel rod was inserted into the L5-6 intervertebral foramen to induce intervertebral foramen stenosis and chronic DRG compression. In the Lipo-$PGE_1$ group, $0.15{\mu}g/kg$ of Lipo-$PGE_1$ were injected intravenously via a tail vein for 10 days starting from the $3^{rd}$ day after operation. Behavioral testing for mechanical and thermal hyperalgesia was performed for 3 weeks after the injections. Results: From the $10^{th}$ day after Lipo-$PGE_1$ injection, the rats in the experimental group showed significant recovery of their mechanical threshold, and this effect was maintained for 3 weeks. No significant differences of the thermal hyperalgesia were observed between the two groups. Conclusions: These findings suggest that intravenously injected Lipo-$PGE_1$ may be effective for alleviating neuropathic pain, which isthe main symptom of spinal stenosis, by improving the blood flow dysfunction.

• The Korean Journal of Pharmacology
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• v.13 no.1 s.21
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• pp.13-21
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• 1977

The author confirmed the development of the smooth muscle in the oviduct proprius and anterior mesosalpinx in the leghorn, and observed that there was a variation between the action of norepinephrine on albumin-secreting portion of productive oviduct and that of non-productive one, and that $PGE_1$ might play a significant role on the activation of adrenergic ${\alpha}$-receptor in the non-productive oviduct. 1. There were many bundles of smooth muscles with irregular directions, which were identified in the both oviduct proprius and anterior mesosalpinx by Mallory aniline-blue orange G stain. 2. In vitro experiments, the anterior mesosalpinx was always relaxed by norepinephrine. While the albumin-secreting portion of non-productive period of oviduct was relaxed, but that of the productive one contracted by norepinephrine. Both the anterior mesosalpinx and oviduct proprius of chick responsed with relaxation to norepinephrine as shown in the non-productive hen. In vivo experiments, norepinephrine injected through the jugular vein increased the intraoviductal pressure in the productive oviduct, but decreased that in the non-productive one. 3. By treatment with $PGE_1$, in vitro, the relaxation induced not only by norepinephrine, but by periarterial electrical stimulation was converted into contraction, and in the presence of phentolamine, this conversion by $PGE_1$ was not shown. 4. The intra-oviductal pressure of the productive hen treated with indomethacin for 4 days was decreased by norepinephrine, but the increase in pressure by $PGE_1$ or $PGE_{2{\alpha}}$ was supersensitized when these drugs were administered through jugular vein. However, in vivo, the relaxation by norepinephrine was not converted into the stimulation after $PGE_1$ treatment. It might be summarized that the regulation of intra-oviductal pressure was dependent on the summation of the movement of both oviduct and mesosalpinx and intramurally produced prostaglandins contributes to the inherent tone of the prcductive oviduct by activating adrenergic ${\alpha}$-receptor.

• Journal of Periodontal and Implant Science
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• v.26 no.4
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• pp.1013-1021
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• 1996

There are many important factors in periodontal inflammation. $IL-1{\beta}$, $PGE_2$ and collagenase are predorminantly key factors. These inflammatory mediators induce gingival tissue and alveolar bone destruction. For the prevention and treatment of periodontal disease, it is necessary to inhibit $IL-1{\beta}$, $PGE_2$ production and collagenase activity. Ursodeoxycholic acid(UDCA) has immunomodulatory properties, and there is evidence that some natural extracts show antiinflammatory activity to some degree. The purpose of this study was to assess the inhibitory effect of UDCA and its mixture with natural extracts on $IL-1{\beta}$, $PGE_2$ production and collagenase activity. Accordingly we assessed the effect of UDCA and its mixture combined with some natural extracts on inhibition of $IL-1{\beta}$, $PGE_2$ production and collagenase activity. For the $IL-l{\beta}$ inhibition study, cultured cells were exposed to $25{\mu}g/ml$ LPS. $IL-1{\beta}$ activity was measured by $IL-1{\beta}$ enzyme immunoassay system. Human gingival fibroblasts were prepared and cells (l05/well) were seeded into culture plates. $rhIL-1{\beta}$ was added to induce $PGE_2$. The amount of $PGE_2$ in sample media was measured using enzyme immunoassay system. Crude collagenase was prepared from Porphyromonas gingivalis and collagenolytic activity was determined using a Collageno kit CLN-100. The test inhibitor was added to the assay mixture consisting of 0.1ml of 50mM Tris buffer(pH 7.5) and 0.2ml of substrate solution. UDCA and UDCA combined with natural extracts generally inhibited $IL-1{\beta}$ production. groups above 0.01% UDCA strongly inhibited $IL-l{\beta}$ synthesis. Both groups inhibited $IL-1{\beta}-induced$ synthesis of $PGE_2$. In low concentration, the degree of inhibition was as same as prednisolone. In high concentration, each group was superior to prednisolone. UDCA group and UDCA mixture group exerted a moderate inhibition of collagenolytic enzyme. The present study suggested that UDCA and its mixture with natural extracts could be further investigated as antiinflammatory drug for periodontal disease.

• Journal of the Korea Convergence Society
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• v.10 no.2
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• pp.331-337
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• 2019

Objective: We studied the effects of 4x, 30x, 30c, and 200c homeopathic dilutions of A. montana on inflammation in primary cultured mouse chondrocytes. Methods: Examined expression of Coll-2 and COX-2, and secretion of PGE2. Results: Treatment with 4x, 30x, and 30c A. montana decreased mRNA expression of Coll-2 and 30x A. montana increased mRNA expression of COX-2, while treatment with 30x and 30c A. montana increased protein expression of COX-2. Treatment with the 30c A. montana increased release of PGE2. Conclusion: Treatment with A. montana induces dedifferentiation and inflammatory responses, including increased COX-2 expression and PGE2 secretion.

• The Korea Journal of Herbology
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• v.32 no.2
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• pp.49-56
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• 2017

Objectives : This study investigated the anti-oxidant activities and improving effect of Phellinus linteus and Glycyrrhiza uralensis Extract (PGE) on Atopic Dermatitis. Methods : 2,2′-diphenyl-1-picrylhydrazyl (DPPH) radical, 2,2′-azino-bis 3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical, Hydrogen peroxides scavenging activities and Superoxide dismutase (SOD)-like activities were used for the measurement of anti-oxidant ability. Cytotoxicity of PGE in Raw 264.7 cell was evaluated by MTT assay. To evaluate the anti-atopic dermatitis effect of PGE, a total of 33 patients with atopic dermatitis were observed trans epidermal water loss, skin moisture content, modified SCORAD index of atopic dermatitis and pruritic degree after applying the PGE for 4 weeks. Results : PGE scavenged DPPH ($IC_{50}=25ppm$) effectively, ABTS and Hydrogenperoxides scavenged similar to BHA. As for the SOD-like activity, it had lower effect than ascorbic acid, but it comparable activities in 500ppm. There was no cytotoxicity at PGE at concentrations of 10,000ppm. In clinical research about PGE on patients with atopic dermatitis, skin condition was improved. After 4 weeks, the application of PGE increased skin moisture content from 19.43 to 31.22. Moreover, it reduced the skin temperature (from 32.5 to 31.9), skin pH (from 5.39 to 5.22), trans epidermal water loss (from 39.03 to 24.46) and pruritus score (from 6.07 to 3.87). In addition, the Modified SCORAD index decreased from 31.28 to 20.3. Conclusions : In conclusion, PGE possesses anti-oxidant and anti-atopic dermatitis activities, thus it could be potentially valuable as anti-atopic dermatitis material.

• The korean journal of orthodontics
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• v.42 no.3
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• pp.118-128
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• 2012

Objective: The aim of this study was to investigate and compare the in vivo effects of prostaglandin E2 (PGE2) administered by different methods on orthodontic tooth movement and bone metabolism macroscopically, histopatologically, and biochemically. Methods: Forty-five young adult New Zealand rabbits were randomly divided into 3 experimental groups (n = 10/group), 1 positive control group (n = 10), and 1 negative control group (n = 5). The experimental rabbits were fitted with springs exerting 20-g reciprocal force on the maxillary incisors and PGE2 (10 ${\mu}g/mL$) was administered by the intravenous, submucosal, or intra ligamentous route aft er appliance insertion and on days 1, 3, 7, and 14 thereafter. All rabbits were sacrificed on day 21 and their premaxillae were resected for histologic evaluation. Results: Tooth movement was observed in the experimental and positive control groups, but the intraligamentous PGE2 group had the highest values of all analyzed parameters, including serum calcium and phosphorus levels and osteoclastic and osteoblastic populations (p < 0.001). Conclusions: Sub mucosal and intraligamentous PGE2 administration significantly increases orthodontic tooth movement and bone metabolism, but the intraligamentous route seems to be more effective.