• Title/Summary/Keyword: prostaglandin

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Effects of Prostaglandins on Embryonic Expansion and Hatching by Developmental Stage in Mouse (발생단계에 따라 Prostaglandins가 생쥐배아의 팽창과 부화에 미치는 영향)

  • 전용필;김정훈;윤용달;김문규
    • Development and Reproduction
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    • v.2 no.2
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    • pp.179-187
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    • 1998
  • The effects of prostaglandins in hatching and implantation have been studied but the results were various, and those are not well known by the embryonic stage. The present study examined the effects of prostaglandin $E_2$(PG $E_2$) and prostaglandin $F_2$$_{\alpha}$ (PG $F_2$$_{\alpha}$) on the expansion and hatching of mouse embryos by embryonic stage. Also we tried to measure the concentration of prostaglandins of morula, expanded, and hatching embryos. In early morula stage embryos, high concentration of PG $E_2$(>100$\mu$M) showed cytotoxicity but PG $F_2$$_{\alpha}$ did not. The hatching was inhibited all groups but not gave negative effects on expansion. In 84 hr and 96 hr stage embryos, the hatching rate was decreased at all treatment groups but not inhibited the expansion. When combine prostaglandin with indomethacin, the hatching rate was increased significantly compared to the prostaglandin-treated groups, and as lower and lower the PG $E_2$ concentration, the hatching rate increased to the control level. The embryonic synthesis of PG $E_2$ increased dramatically but that of PG $F_2$$_{\alpha}$ increased gradually. PG $E_2$ showed cytotoxicity at early stage embryos much than late stage embryos, but PG $F_2$$_{\alpha}$ did not. Hatching was inhibited by the high PG $F_2$$_{\alpha}$ concentration. It is suggested that the inhibition of hatching might be at resulted from cytotoxicity of PG $E_2$ on embryo. However, it is thought that the mechanisms of inhibition of hatching are different between PG $E_2$ and PG $F_2$$_{\alpha}$. In conclusion, it can be suggested that PG $E_2$ and PG $F_2$$_{\alpha}$ concerned with the expansion and hatching, and their effects on hatching were different by the embryonic stage.$/ concerned with the expansion and hatching, and their effects on hatching were different by the embryonic stage.

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Prostaglandin in Regulations of Renal Blood Flow during Partial Ureteral Obstruction in Dogs

  • Song, Hoo-Bin;Yang, Hun-Mo;Min, Young-Gi
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.1
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    • pp.77-84
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    • 1998
  • Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.

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Development of a Coupled Enzyme Assay Method for Microsomal Prostaglandin E Synthase Activity

  • Choi, Kyung-A;Park, Sung-Jun;Yu, Yeon-Gyu
    • Bulletin of the Korean Chemical Society
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    • v.31 no.2
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    • pp.384-388
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    • 2010
  • Human microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the conversion of prostaglandin $H_2$ ($PGH_2$) into prostaglandin $E_2$ ($PGE_2$). To establish a stable and efficient method to assess the activity of mPGES-1, a coupled enzyme assay system using mPGES-1, 15-hydroxyprostaglandin dehydrogenase (15-PGDH) and phosphomolybdic acid (PMA) was developed. In this assay system, $PGH_2$ was converted to $PGE_2$ by mPGES-1, and then $PGE_2$ was further transformed to the 15-keto-$PGE_2$ by 15-PGDH accompanying the production of NADH, which was easily detected by fluorescence spectrometry in a multi-well plate format. During the reaction, spontaneous oxidation of $PGH_2$ was prevented by PMA. Using this novel assay, the $K_m$ value of mPGES-1 for $PGH_2$ and the $IC_{50}$ value of the previously characterized inhibitor, MK-886, were determined to be 0.150 mM and $2.8\;{\mu}M$, respectively, which were consistent with the previously reported values. In addition, low backgrounds were observed in the multi-wall plate screening of chemical compounds.

The Protective Effect of Prostaglandin E1 Against Ischemia-reperfusion Injury of Musculocutaneous Flaps (백서 복직근피판에 있어 허혈-재혈류 손상에 미치는 Prostaglandin E1의 예방효과)

  • Hong, Joon Pio;Chung, Yoon Kyu;Chung, Soon-Hee
    • Archives of Reconstructive Microsurgery
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    • v.9 no.2
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    • pp.190-198
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    • 2000
  • 본 연구는 백서 복직근피판에 있어 허혈-재혈류 손상에 미치는 prostaglandin E1(PGE-1)의 예방효과를 분석 실험하였으며, 그 기전으로 내피세포의 intercellular adhesion molecule-1(ICAM-1)이 down regulation 됨을 확인하였다. 기존의 PGE-1은 혈관 확장 및 혈소판 응고 저하 등의 기전으로 피판 이식술 후 주로 사용하였으나, 허혈-재혈류 손상 시에 PGE-1 역할에 대한 연구는 잘 알려진바 없다. 허혈-재혈류 손상에 대한 기전은 현재 여러 가설로 설명되고 있으나, 최근 내피 세포와 백혈구의 역할이 주목을 받고 있다. 장시간 허혈 상태의 피판은 재혈류시 백혈구가 내피세포에 접착함으로써 직간접적인 경로로 독소를 생성하며, 결국 내피세포 및 주변조직의 괴사로 이어진다. 본 연구는 면역조직학 염색을 통한 내피세포의 ICAM-1 발현 억제와 그로 인한 백혈구의 내피세포 접착 억제를 그 기전으로 볼 수 있었으며, PGE-1을 술 중 투여함으로써 피판의 생존율을 향상시킬 수 있었다.

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Prostaglandin E Synthase, a Terminal Enzyme for Prostaglandin E2 Biosynthesis

  • Kudo, Ichiro;Murakami, Makoto
    • BMB Reports
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    • v.38 no.6
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    • pp.633-638
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    • 2005
  • Biosynthesis of prostanoids is regulated by three sequential enzymatic steps, namely phospholipase $A_2$ enzymes, cyclooxygenase (COX) enzymes, and various lineage-specific terminal prostanoid synthases. Prostaglandin E synthase (PGES), which isomerizes COX-derived $PGH_2$ specifically to $PGE_2$, occurs in multiple forms with distinct enzymatic properties, expressions, localizations and functions. Two of them are membrane-bound enzymes and have been designated as mPGES-1 and mPGES-2. mPGES-1 is a perinuclear protein that is markedly induced by proinflammatory stimuli, is down-regulated by anti inflammatory glucocorticoids, and is functionally coupled with COX-2 in marked preference to COX-1. Recent gene targeting studies of mPGES-1 have revealed that this enzyme represents a novel target for anti-inflammatory and anti-cancer drugs. mPGES-2 is synthesized as a Golgi membrane-associated protein, and the proteolytic removal of the N-terminal hydrophobic domain leads to the formation of a mature cytosolic enzyme. This enzyme is rather constitutively expressed in various cells and tissues and is functionally coupled with both COX-1 and COX-2. Cytosolic PGES (cPGES) is constitutively expressed in a wide variety of cells and is functionally linked to COX-1 to promote immediate $PGE_2$ production. This review highlights the latest understanding of the expression, regulation and functions of these three PGES enzymes.

Experience of Administering Oral Prostaglandin E1 for Failed Back Surgery Syndrome -A case report- (척추수술후증후군 환자에서 경구용 Prostaglandin E1에 의한 치료 경험 -증례보고-)

  • Lee, Hae Kwang;Woo, Seung Hoon;Lee, Woo Yong
    • The Korean Journal of Pain
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    • v.19 no.1
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    • pp.101-103
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    • 2006
  • Oral prostaglandin E1 (PGE1) is a medicine that is clinically applied during a treatment of patients suffering with vascular disease with chronic arterial obstruction because it has vasodilation and anti-platelet effects. The mechanisms of lumbosacral symptoms associated with spinal stenosis probably include vascular insufficiency with hypoxic injury to the cauda equina and the nerve roots. Thus, increasing the blood supply would be beneficial to improve the pathophysiologic condition. Several studies on the improvement of clinical symptoms of spinal stenosis by PGE1 treatment have been reported on. In this case, 47-year old female underwent posterior compression and posterolateral fusion with a cage at L2-4 due to L3 compression fracture, and she did not show improvement of the radiating pain of her right leg after the operation. Therefore, she received repetitive epidural catheterization and adhesiolysis, epidural block and physical therapy, but her symptoms deteriorated after temporary improvement. Finally, she was given PGE1 and the radiculopathy was completely improved, although some muscle weakness still remained.

Control of parturition time on Pig 4. Effect of prostaglandin $F_2{\alpha}$ on uterine smooth muscle motility (돼지 분만시기의 조절에 관하여 4. 자궁평활근의 운동성에 대한 Prostaglandin $F_2{\alpha}$의 영향)

  • 심철수;정성진;이양성;임종옥
    • Korean Journal of Veterinary Service
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    • v.18 no.3
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    • pp.29-35
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    • 1995
  • The effects of prostaglandin $F_2{\alpha}$ were investigated on the uterine smooth muscle motility in the pig. The results were summarized as follows : 1. Prostaglandin $F_2{\alpha}$ caused the contraction of the porcine uterine smooth muscle and the contractile responses increased between the concentration of prostaglandine $F_2{\alpha}$ $10^{-9}$ M and $5{\times}10^{-8}$ M with a dose-dependent manner. 2. The contractile response induced by prostaglandine $F_2{\alpha}$($10^{-8}$ M) was not blocked by pre-treatment with cholinergic receptor blocker, atropine ($10^{-6}$ M). 3. The contractile response induced by prostaglandine $F_2{\alpha}$(10$^{-8}$ M) was not blocked by pretreament with ${\alpha}$-adrenergic receptor blocker, phentolamine($10^{-6}$ M) and ${\beta}$-adrenergic receptor blocker, propranolol($10^{-6}$ M). From these results, it was concluded that the effects of uterine smooth muscle by prostaglandine $F_2{\alpha}$ were only the contraction mediated by prostaglandine TEX>$F_2{\alpha}$ receptor in pig, and that it may not be related to the cholinergic and adrenergic receptor.

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