• Title/Summary/Keyword: Prostaglandin $D_2$

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THE EFFECT OF INDOMETHACIN ON PROSTAGLANDINS IN 4-NITROQUINOLINE-N-OXIDE (4-NQO) INDUCED PALATAL CARCINOMA OF ALBINO RATS (Indomethacin이 4-Nitroquinoline-N-Oxide(4-NQO) 유도 백서 구개암 발암과정에서 prostaglandins에 미치는 영향에 관한 연구)

  • Kim, Young-Soo
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.11 no.1
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    • pp.187-202
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    • 1989
  • This study was undertaken to investigate the effect of indomethacin on prostaglandins in 4-Nitroquinoline-N-Oxide (4-NQO) induced palatal carcinoma of albino rats. 128 Sprague-Dawley strain albino rats-about 100g in body weight-were used in this study, divided into as belows; 1. Normal group (16-albino rats) with no treatment, 2. Control group (16-albino rats) treated with prophylene application onto palatal mucosa 3 times a week. 3. Experimental group I (48-albino rats) treated with 0.5% 4-NQO in prophylene application onto palatal mucosa 3 times a week. 4. Experimental group II (48-albino rats) treated with 0.5% 4-NQO in prophylene application with administered $20{\mu}g/ml$ of indomethacin in drinking water ad. lib. Four animals were sacrificed 7th, 13th, 19th, and 25th week respectively in normal and control group, and 7th, 9th, 11th, 13th, 15th, 17th, 19th, 21st, 23rd, 25th, 27th and 29th week respectively in experimental group I and II at each time. The palatal and lingual tissues were excised and kept frozen at $-70^{\circ}C$. Densitometer scan and Beta-counting counter were used for the thin layer chromatography of the arachidonic acid metabolites. The obtained results were as belows; 1. In normal and control group, there was little change of the arachidonic acid metabolites during experiment period, and the tissue homogenates included prostaglandin $D_2$, 6-keto-prostaglandin $F_{1{\alpha}}$, prostaglandin $E_2$, thromboxane $B_2$, prostaglandin $F_{2{\alpha}}$ in that order of relative abundances. 2. In experimental group I, prostaglandin $D_2$, and prostaglandin $E_2$ were increased, while 6-keto-prostaglandin $F_{1{\alpha}}$ and thromboxane $B_2$ were decreased in relative abundances of arachidonic acid metabolites. And there was little change in prostaglandin $F_{1{\alpha}}$ 3. In experimental group II, prostaglandin $D_2$, and prostaglandin $E_2$ were increased, while 6-keto-prostaglandin $F_{1{\alpha}}$ and thromboxane $B_2$ were decreased in relative abundances of arachidonic acid metabolites. And there was little change in prostaglandin $F_{2{\alpha}}$ also. 4. In the range of increase in prostaglandin $D_2$, and prostaglandin $E_2$, and that of decrease in 6-keto-prostaglandin $F_{1{\alpha}}$ and thromboxane $B_2$, in relative abundances, there was wider in experimental group I than in group II. 5. In the range of increase in prostaglandin $D_2$, and prostaglandin $E_2$, and that of decrease in 6-keto-prostaglandin $F_{1{\alpha}}$ and thromboxane $B_2$, in relative abundances, there was wider in palatal mucosa than in lingual mucosa in experimental group I and II.

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Effects of Bacterial Lipopolysaccharide on Prostaglandin Production in Primary Cultured Rat Vascular Smooth Muscle Cells (일차 배양 랫드 혈관 평활근 세포에서 Prostaglandin 생성에 미치는 Bacterial Lipopolysaccharide의 작용 특성)

  • 이수환
    • Journal of Food Hygiene and Safety
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    • v.11 no.4
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    • pp.227-234
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    • 1996
  • This study was designed to characterize endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). The time course for prostaglandin synthesis in lipopolysaccharide (LPS)-stimulated VSMC showed that the maximum production was reached in 12 hours. LPS induced prostaglandin H2 synthase (PGHS) activity in VSMC and the time course profile in the changes of PGHS activity paralleled that of total prostaglandin production. Differential treatment showed that 4 hours' exposure to LPS was enough for the maximum effect on the prostaglandin production and this effect was completely inhibited by the co-treatment of actinomycin D, a transcription inhibitor. These results suggest that LPS effect might be determined within 4 hours. Actinomycin D increased PGHS activity without affecting prostaglandin production if added 4 hours after LPS treatment. On the other hand, cyclogeximide, a translation inhibitor, augmented LPS-induced prostaglandin production if treated during first four hours, but it inhibited LPS-induced PGHS activity regardless of treatment schedule. These results suggest the existence of multiple regulating mechanisms in the LPS-induced prostaglandin synthesis.

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Effects of Cyclobuxine D on the Biosynthesis of Prostaglandins in Vitro, Prostaglandins Production and Leukocyte Migration in Vivo (Cyclobuxine D의 prostaglandin 합성과 백혈구 유주에 미치는 영향)

  • Lee, Jong-Hwoa;Park, Young-Hyun;Cho, Byung-Heon;Kim, Yu-Jae;Kim, Jong-Bae;Kim, Chung-Mok;Kim, Chun-Sook;Cha, Young-Deog;Kim, Young-Suk
    • The Korean Journal of Pharmacology
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    • v.23 no.1
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    • pp.51-56
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    • 1987
  • Cyclobuxine D was extracted from Buxus microphylla var. koreana Nakai. The effects of cyclobuxine D on the biosynthesis of prostaglandins from arachidonic acid in guinea pig lung, prostaglandin production and leukocyte migration in carrageenin-induced inflammation was investigated. These effects of cyclobuxine D were compared with those of aspirin and dexamethasone. Cyclobuxine D does not inhibit significantly cyclooxygenase in guinea pig lung but reduces prostaglandin concentration and leukocyte migration in inflammatory exudates. These effects of cyclobuxine D differ from that of aspirin which inhibits biosynthesis of prostaglandin in vitro and has a relative small effect on leukocyte migration. Dexamethasone, which does not inhibit cyclooxygenase in vitro, has an effect similar to that of cyclobuxine D on leukocyte migration and prostaglandin production in inflammatory exudates.

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15-DEoxy-$d^{12,14}$ Prostaglandin $J_2$ Rescues Pc12 Cells From Hydrogen Peroxide-induced Apoptosis Through Upregulation Of Heme Oxygenase-1

  • Kim, Ji-Woo;Jang, Jung-Hee;Surh, Young-Joon
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.153.1-153.1
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    • 2003
  • Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. l5-Deoxy-$D^{12, 14}$ prostaglandin $J_2$ (15d-$PGJ_2$), a dehydration product of prostaglandin $D_2$, has been reportd to possess a number of biological activities such as anti-inflammatory, anticarcinogenic, and antioxidative properties. (omitted)

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The Effects of Bee Venom on PLA2, COX-2, iNOS, AA and PG in RAW 264.7 Cells (봉약침액(蜂藥鍼液)이 PLA2, COX-2, iNOS, AA 및 미치는 영향(影響)에 관(關)한 연구(硏究))

  • Ha, Seang-Jong;Lee, Seong-No;Jo, Hyun-Chul;Kim, Kee-Hyun
    • Journal of Pharmacopuncture
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    • v.5 no.2
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    • pp.40-51
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    • 2002
  • Objectives : The purpose of this study was to investigate the effect of Bee Venom on the lipopolysaccharide-induced expression phospholipase $A_2$, cyclooxygenase-2 and inducible nitrogen oxide synthase, and the generation of arachidonic acid, prostaglandin D2 and E2 in RAW 264.7 cells, a murine macrophage cell line. Methods : The expression of phospholipase $A_2$, cyclooxygenase and inducible nitrogen oxide synthase was determined by western blotting with corresponding antibodies, and the generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ was assayed by ELISA method in RAW 264.7 cells. The non-toxic concentrations (0.1 to $5\;{\mu}g/ml$) of bee venom determined by MTT assay, were used in this study. Results : 1. Bee venom inhibited lipopolysaccharide-induced expression of phospholipase $A_2$ in a dose dependent manner after 48 hours treatment. 2. Bee venom inhibited lipopolysaccharide-induced expression of cyclooxygenase-2 in a dose dependent manner after 24 and 48 hours treatment. 3. Bee venom inhibited lipopolysaccharide-induced expression of inducible nitrogen oxidesynthase in a dose dependent manner after 48 hours treatment. 4. The generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ was not much affected by the treatment of bee venom on the lipopolysaccharide-induced generation of arachidonic acid, prostaglandin $D_2$ and $E_2$ in RAW 264.7 cells.

The Effects of 120Hz Electroacupuncture on the Prostaglandin E2 and Spinal N-Methyl-D-Aspartate Receptor Expression in the Carrageenan-Injected Rat (고빈도 120 Hz 전침이 Carrageenan으로 유발된 흰쥐의 Prostaglandin E2와 척수 N-Methyl-D-Aspartate Receptor 발현에 미치는 영향)

  • Son, In-seok;Choi, Byung-tae;Jang, Kyung-jeon
    • Journal of Acupuncture Research
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    • v.20 no.3
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    • pp.15-23
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    • 2003
  • Objective : The role of high frequency 120 Hz electroacupuncture(EA) in carrageenan-induced pain was studied by examining the alnalgesic effects, and prostaglandin $E_2(PGE_2)$ levels measurement and spinal N-methyl-D-aspartate(NMDA) receptor expression. Inflammation was induced by an intraplantar injection of 1% carrageenan into the right hind paw. Method : Bilateral EA stimulation with 120 Hz were delivered at those acupoints corresponding to Zusanli and Sanyinjiao in man via the needles for a total of 30 min duration in carrageenan-injected rats. Results : EA stimulation showed significant analgesic effects as measured by analgesy-meter at all time points tested compared with controls. Three hours after carrageenan injection, PGE2 levels were measured by commercial kit. EA significantly inhibited PGE2 production in the right paw. The number of NR1 and NR2A, NMDA receptor, immunoreactive neurons was significantly increased in the superficial dorsal horn(laminae I-II) and nucleus proprius(laminae III-IV) of ipsilateral spinal cord at L4-5. But the number of carrageenan-induced NR1 and NR2A immunoreactive neuron, especially NR1 immunoreaction in the superficial dorsal horn, was reduced by 120 Hz EA stimulation. Conclusions : These results indicate that NMDA receptors may mediate transmission of nociceptive information originating in tissue inflammation of hind paw and high frequency 120 Hz EA stimulation have an alleviating action against local inflammatory pain.

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The physiological and pharmacological roles of prostaglandins in hair growth

  • Shin, Dong Wook
    • The Korean Journal of Physiology and Pharmacology
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    • v.26 no.6
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    • pp.405-413
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    • 2022
  • Hair loss is a common status found among people of all ages. Since the role of hair is much more related to culture and individual identity, hair loss can have a great influence on well-being and quality of life. It is a disorder that is observed in only scalp patients with androgenetic alopecia (AGA) or alopecia areata caused by stress or immune response abnormalities. Food and Drug Administration (FDA)-approved therapeutic medicines such as finasteride, and minoxidil improve hair loss temporarily, but when they stop, they have a limitation in that hair loss occurs again. As an alternative strategy for improving hair growth, many studies reported that there is a relationship between the expression levels of prostaglandins (PGs) and hair growth. Four major PGs such as prostaglandin D2 (PGD22), prostaglandin I2 (PGI2), prostaglandin E2 (PGE2), and prostaglandin F2 alpha (PGF) are spatiotemporally expressed in hair follicles and are implicated in hair loss. This review investigated the physiological roles and pharmacological interventions of the PGs in the pathogenesis of hair loss and provided these novel insights for clinical therapeutics for patients suffering from alopecia.

Possible Role of Heme Oxygenase-1 and Prostaglandins in the Pathogenesis of Cerebral Malaria: Heme Oxygenase-1 Induction by Prostaglandin $D_2$ and Metabolite by a Human Astrocyte Cell Line

  • Kuesap, Jiraporn;Na-Bangchang, Kesara
    • Parasites, Hosts and Diseases
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    • v.48 no.1
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    • pp.15-21
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    • 2010
  • Astrocytes are the most abundant cells in the central nervous system that play roles in maintaining the blood-brain-barrier and in neural injury, including cerebral malaria, a severe complication of Plasmodium falciparum infection. Prostaglandin (PG) $D_2$ is abundantly produced in the brain and regulates the sleep response. Moreover, $PGD_2$ is a potential factor derived from P. falciparum within erythrocytes. Heme oxygenase-1 (HO-1) is catalyzing enzyme in heme breakdown process to release iron, carbon monoxide, and biliverdin/bilirubin, and may influence iron supply to the P. falciparum parasites. Here, we showed that treatment of a human astrocyte cell line, CCF-STTG1, with $PGD_2$ significantly increased the expression levels of HO-1 mRNA by RT-PCR. Western blot analysis showed that $PGD_2$ treatment increased the level of HO-1 protein, in a dose- and time-dependent manner. Thus, $PGD_2$ may be involved in the pathogenesis of cerebral malaria by inducing HO-1 expression in malaria patients.

Effect of Blood Concentrations of Free Unsaturated Fatty Acid, Phospholipid, Creatinine and Prostaglandin on the Stages of Pregnancy and Parturition in Female Rats (임신과 분만에 따른 흰쥐의 혈액내 유리불포화지방산, 인지질, Creatinine 및 Prostaglandin 함량의 변화)

  • Kim, Young Hong
    • Current Research on Agriculture and Life Sciences
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    • v.3
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    • pp.174-180
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    • 1985
  • This study is designed to evaluate serum free unsaturated fatty acid, phospholipid, creatinine and prostaglandin concentrations to provide normal values for physiological barometers and preliminary information related to these chemical components on the stages of pregnancy and parturition in female rats. Forty female rats are devided into 8 groups. One control group contains 5 intact, nonpregnant female rats and the other 5 pregnancy groups contains each of 5 pregnant rats which are 9, 12, 15, 18 and 21days after pregnancy. The remaining 2 parturition groups contain each of 5 postparturient rats which are 12 and 36 hours after parturition. The results obtained are as follows ; 1. The mean concentrations of free unsaturated fatty acid in serum of the female rats ranges from 6.47 to 8.22 mg/dl. The level of pregnancy group that is 21 days being lower. 2. The mean concentrations of phospholipid in serum of the female rats ranges from 86 to 105 mg/dl. There is no marked difference between all of these groups, especially the levels of 12 days after pregnancy group and 36 hours after parturition group are lower than those of other groups. 3. The mean concentrations of crecatinine in serum of the female rats ranges from 0.64 to 0.84 mg/dl. There is no marked difference between all of 8 groups and the levels of 21 days after pregnancy group are higher than those of other groups. 4. The mean concentrations of prostaglandin in blood of the female rats rarges from 324 to $1208pg/m{\ell}$ and increases from $736pg/m{\ell}$ (18 days after pregnancy) to maximal levels of $1208pg/m{\ell}$ immediately after parturition. and then decreased progressively. Especially, each mean concentration of prostaglandin on 9, 12, or 15 days after pregnancy and mean concentrations of 5 pregnant groups are lower than those of nonpregnant female rats. 5. It is suggested that serum concentrations of free unsaturated fatty acid, phospholipid and creatinine in female rats are not related to the stages of pregnancy and parturition but prostaglandin concentrations influence the initiation of parturition in this species.

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Peroxisome proliferator-activated receptor γ is essential for secretion of ANP induced by prostaglandin D2 in the beating rat atrium

  • Zhang, Ying;Li, Xiang;Liu, Li-Ping;Hong, Lan;Liu, Xia;Zhang, Bo;Wu, Cheng-Zhe;Cui, Xun
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.3
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    • pp.293-300
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    • 2017
  • Prostaglandin $D_2$ ($PGD_2$) may act against myocardial ischemia-reperfusion (I/R) injury and play an anti-inflammatory role in the heart. Although the effect of $PGD_2$ in regulation of ANP secretion of the atrium was reported, the mechanisms involved are not clearly identified. The aim of the present study was to investigate whether $PGD_2$ can regulate ANP secretion in the isolated perfused beating rat atrium, and its underlying mechanisms. $PGD_2$ (0.1 to $10{\mu}M$) significantly increased atrial ANP secretion concomitantly with positive inotropy in a dose-dependent manner. Effects of $PGD_2$ on atrial ANP secretion and mechanical dynamics were abolished by AH-6809 ($1.0{\mu}M$) and AL-8810 ($1.0{\mu}M$), $PGD_2$ and prostaglandin $F2{\alpha}$ ($PGF2{\alpha}$) receptor antagonists, respectively. Moreover, $PGD_2$ clearly upregulated atrial peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and the $PGD_2$ metabolite 15-deoxy-${\Delta}12$, 14-$PGJ_2$ (15d-$PGJ_2$, $0.1{\mu}M$) dramatically increased atrial ANP secretion. Increased ANP secretions induced by $PGD_2$ and 15d-$PGJ_2$ were completely blocked by the $PPAR{\gamma}$ antagonist GW9662 ($0.1{\mu}M$). PD98059 ($10.0{\mu}M$) and LY294002 ($1.0{\mu}M$), antagonists of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling, respectively, significantly attenuated the increase of atrial ANP secretion by $PGD_2$. These results indicated that $PGD_2$ stimulated atrial ANP secretion and promoted positive inotropy by activating $PPAR{\gamma}$ in beating rat atria. MAPK/ERK and PI3K/Akt signaling pathways were each partially involved in regulating $PGD_2$-induced atrial ANP secretion.