• Title/Summary/Keyword: Phosphodiesterase inhibitor

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Progesterone Production and Oocyte Maturatf on of Frog (Rona nigromaculata and Rana rugoBa) Follicles in vitro (참개구리와 옴개구리 여포의 프로제스테론 생성과 난자의 성숙)

  • 권혁방;김지열;고선근
    • The Korean Journal of Zoology
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    • v.33 no.2
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    • pp.175-182
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    • 1990
  • Progesterone production and oocyte maturation in ovarian follicles of Rana nigromaculata and Rana rugosa were investigated. Addition of frog pituitary homogenate (FPH) to the in utiro cultured follicles of R. nigromaculata stimulated a marked increase in the accumulation and secretion of progesterone (P$_4$) by the follicles and induced their oocyte maturation (germinal vesicle breakdown, GVBD) in a dose dependent manner. The FPH (0.1 pituitary equivalent/2 ml)-inducted P4 peak appeared in 3-6 hours and followed by the oocyte GVBD in 9-12 hours after the hormone stimulation. lncreae of intrafollicular cAMP levels with forskolin (an adenylatecyclase stimulator) and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor) mimic the FPH action in the stimulation of P$_4$ production but not in the induction of oocyte maturation. The in uitro cultured follicies of R. rugosa behaved very differently from other amphibian follicles. Addition of FPH-(0. 1 pit. equivl2 ml) to the culture medium neither stimulated P$_4$ production by the follicles nor induced the oocyte GVBD. However, treatment of the follicles with forskolin and IBMX drastically stimulated both the intrafollicular accumulation (800 pg/follicle) and secretion (1700 pg/follicle) of P$_4$ by the follicles during culture period. Thus, the data suggest that the follicles are ready to respond to cAMP increase but not to the FPH stimulation in terms of P$_4$ production.

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Pre-and Post-ishemic Changes of the Constituent Enzymes in Isolated Rabbit's Myocardium (허혈전후 적출 가토 심근내의 구성 효소의 변화)

  • 천수봉;전도환;이재성;김송명
    • Journal of Chest Surgery
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    • v.33 no.2
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    • pp.117-124
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    • 2000
  • Background: Nucleoside transport inhibitor(NTI) Keeps AMP, ADP, ATP levels high in myocytes by inhibiting adenosine cataboilsm so that it may preserve the myocardial contractability during ischemia In this study we investigated the effects of cyclic AMP phosphodiesterase inhibor(C-AMP PDSI) and S-P-nitrobenzyl-6 -thioniosine(NBT; a sort of NIT) on myocadial preservation and changes of constituent enzyme. Material and method: Twenty-six isolated rabbit hearts were perfused with Krebs-Henseleit buffer solution for 20 minutes arrested for 20 minutes and ten reperfused for 30 minutes. The following four groups were prepared and hemodynamic changes coronary effluent lactate dehydrogenase (LDH) a-hydroxybutylic accid(a-HBD) levels and myocardial LDH creatine kinase-MB (CK-MB) adenosine deaminase(ADA) a-HBD levels and myocardial LDH creatine kinase-MB (CK-MB) adenosine deaminase(ADA) a-HBD levels were analysed before and after cardiac arest ; Group I(control) ; the heart was only perfused with K-H ; Group II ; the heart was perfused with K-H including C-AMP PDSI(Amrinone 25mg/L); Group III ; the heart was perfused with K-H including NBT(4.19mg/L) ; Group IV ; the heart was perfused with K-H including C-AMP PDSI + NBT. Result : Left venticular developed pressure(LVDP) at 10 minutes of the equilibrium was significantly higher in group III(72.1$\pm$5.3 mmHg p<0.01) and group III(72$\pm$5.6 mmHg P<0.025) as compared with group I (40.8$\pm$4.7mmHg) and LVDP at 20 minutes of the reperfusion was significantly higher in group II(74$\pm$5.3mmHg p<0.01) and group III(72$\pm$5.6mmHg p<0.025) as compared with group I (44.2$\pm$4.6mmHg). Percentage recovery of LVDP at the reperfusion was the highest in group II(123.3%) Percentage recovery of coronary flow at the equilibrium reperfusion were higher in group II(310%, 270%) group III(230%, 290%) group IV(310%, 280%) as compared with group I (100%) respectively. Myocadial LDH level was significant lower in group IV(33495$\pm$1802 IU/gm p<0.04) as compared with group I(48767$\pm$1421 IU/gm) Myocadial CK-MB level was significant higher in group II(74820$\pm$1421 IU/gm) compared with group I (45450$\pm$1737 IU/gm) Myocadial ADA level was significant higher group IV(1215$\pm$8 IU/gm p<0.05) compared with group I(125$\pm$15 IU/gm) but there was no significant difference between group I and group II ,III, IV in changes of coronary effluent LDH, a-HBD levels. Conclusion: C-AMP PDSI solely appears to have a better effect on myocardial preservation after ischemia than NBT but with no synergistic effect and it could keep CK-MB leve high in myocardial tissues.

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Monitoring of illegal compounds and prohibited natural ingredients in foods (식품 중 발기부전치료제 및 사용금지 성분 모니터링)

  • Yun, Jisuk;Choi, Jangduck;Kwon, Kisung;Jo, Cheon-Ho
    • Korean Journal of Food Science and Technology
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    • v.48 no.5
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    • pp.405-412
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    • 2016
  • Illegally adulterated compounds, such as impotency drugs and their synthetic analogues, which have been purported to enhance sexual potency or mood, have been constantly detected in foods including dietary supplements. The adulterated foods with these illegal compounds may threaten public health because their safety and efficacy have not been verified. This study was aimed at investigating illegal compounds in foods and counterfeit products. 54 illegal compounds were assayed using a simultaneous analytical method involving liquid chromatography equipped with photo diode array (LC-PDA) and LC coupled with tandem mass spectrometry (LC-MS/MS). The method was validated in terms of selectivity, linearity, limit of detection (LOD), limit of quantification (LOQ), precision and accuracy. In 48 of 161 samples, we identified 7 different illegal compounds, including sildenafil, tadalafil, chlropretadalafil, demethylsildenafil, dimethyl-thiosildenafil, icariin and yohimbine. When purchasing products marketed for erectile dysfunction or aphrodisiacs, ulmost care should be taken owing to the possible presence of these illegal compounds.

Effects of Sinetrol-XPur on Leptin-Deficient Obese Mice and Activation of cAMP-Dependent UCP-2 (Leptin 유전자 결핍 동물모델을 이용한 시네트롤(Sinetrol-XPur)의 항비만 효과와 cAMP를 통한 UCP-2 활성화 기전 연구)

  • Yoo, Jae Myeong;Lee, Minhee;Kwon, Han Ol;Choi, Sei Gyu;Bae, Mun Hyoung;Kim, Ok-Kyung
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.45 no.4
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    • pp.484-491
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    • 2016
  • The present study investigated the effect of Sinetrol-XPur (polyphenolic Citrus spp. and Paullinia cupana Kunth dry extract) and defined the action mode for cyclic adenosine monophosphate (cAMP)-dependent uncoupling protein (UCP)-2 activation. Leptin-deficient obese mice were treated with two different doses, 100 mg/kg body weight (BW) and 300 mg/kg BW of each AIN93G supplement, for 7 weeks. Treatment of obese mice with both low and high doses of Sinetrol-XPur significantly reduced body weight gain compared to control obese mice. White adipose tissue weight of mice was reduced by 30.96% in high dose-supplemented groups. Serum total cholesterol and triglyceride were reduced by a high dose of Sinetrol-XPur by 20.02% and 30.96%, respectively. Serum level of high density lipoprotein (HDL) was significantly increased by treatment with both doses, as the ratio of HDL to low density lipoprotein increased by 138.78% and 171.49%, respectively. Regarding expression of biochemical factors related to lipid metabolism, fatty acid synthase significantly decreased and UCP-2 increased upon treatment with a high dose of Sinetrol-XPur, but there was no significant difference in lipoprotein lipase and hormone-sensitive lipase. To define cellular mechanism, intracellular cAMP levels in 3T3-L1 adipocytes significantly increased in a dose-dependent manner over the range of $50{\sim}250{\mu}m/mL$. The phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine clearly blocked cAMP, suggesting that Sinetrol-XPur promotes lipolysis of adipocytes through inhibition of cAMP-dependent PDE, resulting in induction of cAMP response element binding protein and UCP-2. These results suggest that Sinetrol-XPur supplementation is a viable option for reducing body weight and fat by improving serum lipid profiles and genetic expression of lipid metabolic factors, especially activation of cAMP-dependent UCP-2.