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Efeitos do 17β-estradiol na abundância de transcritos para enzimas envolvidas na síntese de PGF2α endometrial em fêmeas bovinas no final do diestroFeltrin, Isabella Rio January 2020 (has links)
Orientador: Claudia Maria Bertan Membrive / Resumo: Em bovinos, o 17β-estradiol (17β-E2) estimula a expressão de receptores de estradiol (ER) e ocitocina (OXTR) no endométrio. A ativação de OXTR induz a ativação de uma complexa cascata que resulta na síntese de PGF2α. A hipótese é que o tratamento com 17β-E2, 15 dias após o estro (D15), modula a expressão gênica das proteínas quinase (PKC) e fosfolipase A2 (PLA2), ambas envolvidas na síntese de PGF2α e dependentes de cálcio. Objetivou-se neste estudo determinar os efeitos do 17β-E2 na abundância de trancritos (PKCα, PKCβ, PLA2G4, AKR1B1, AKR1C4 e PTGS2) diretamente envolvidos na síntese de PGF2α. Novilhas (N=50), não prenhes, cíclicas, foram sincronizadas pela inserção de um dispositivo de liberação intravaginal contendo 0,558g de progesterona (P4), pela administração de 1 mg de benzoato de estradiol e 0,075 mg de D-Cloprostenol, ambos intramuscular (IM). Após 6 dias, foi injetado 0,075 mg de D-Cloprostenol, IM. Após 48 horas, o dispositivo contendo P4 foi removido e 0,150 mg de D-Cloprostenol foi administrado IM. Nesta ocasião, um adesivo foi inserido na base da cauda para a identificação dos estros (Boviflag Red Estrus Detector - ABS Pecplan) e observações de estro foram realizadas nos próximos 4 dias. Participaram do experimento somente novilhas identificadas em estro (D0 = dia do estro) e que ovularam (N=46). Entre D14 e D23, a área do corpo lúteo (CL; cm2), fluxo sanguíneo (%) e as concentrações plasmáticas de progesterona (P4) foram avaliadas diariamente. No D15, as novi... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: In cattle, 17β-estradiol (17β-E2) stimulates expression of estradiol (ER) and oxytocin receptor (OXTR) in the endometrium. The activation of OXTR leads to the induction of a complex cascade of molecular activation resulting in PGF2α synthesis. The hypothesis was that 17β-E2 treatment on day 15 (D15) after estrus modulates the gene expression of protein kinase (PKC) and phospholipase A2 (PLA2), both directly involved in the synthesis of PGF2α and calcium dependent. The aim of this study was to determine the effects of 17β-E2 on the abundance of key transcripts (PKCα, PKCβ, PLA2G4, AKR1B1, AKR1C4 and PTGS2) involved in PGF2α signaling and synthesis. Nelore heifers (N=50), don't pregnant, cyclic were synchronized by insertion an intravaginal release device containing 0.558g of progesterone (P4), and by the administration of 1 mg of estradiol benzoate and 0.075 mg de D-Cloprostenol, both intramuscularly (IM). After 6 days, 0.075 mg D-Cloprostenol was injected, IM. After 48 hours the P4 device was removed and 0.150 mg D-Cloprostenol was administered IM. On this occasion, an adhesive was inserted at the base of the tail for the identification of estrus (Boviflag Red Estrus Detector - ABS Pecplan) and estrous observation were made in the next 4 days. Participated in the experiment only the heifers identified in estrus (D0 = day of estrus) that ovulated (N=46). Between D14 and D23, corpus luteum (CL) area (cm2), blood flow (%), and progesterone (P4) plasmatic concentrations were eval... (Complete abstract click electronic access below) / Mestre
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Prostaglandin-Mediated Reinstatement of Drug Taking After Alcohol Drinking by Female Adolescent RatsKline, Hannah L. 04 1900 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Adolescent alcohol abuse is a global problem that initiates lifelong addiction.
Alcohol use during adolescence is associated with subsequent Meth dependence in
humans. Specifically, female adolescents are particularly vulnerable to serial alcohol and
Meth use. However, it is unknown if prior voluntary alcohol drinking impacts subsequent
Meth-taking in female adolescent rats. Both alcohol and Meth increase the prostaglandin
synthesis enzyme cyclooxygenase-2 (COX-2) in the brain but the effect of serial exposure
to alcohol and Meth on COX-2 has not been determined. The first study uses a novel
method of serial voluntary alcohol drinking and Meth self-administration in female
adolescent rats to model human patterns of co-abuse. Prior alcohol drinking did not affect
subsequent Meth self-administration, but it reduced the cue-primed reinstatement of Methseeking
after abstinence from Meth. Rats with a history of adolescent alcohol drinking also
had increased COX-2 in the dorsal striatum, regardless of subsequent Meth selfadministration.
These findings demonstrate that a history of adolescent alcohol drinking
does not alter Meth self-administration but persistently reduces cue-primed Meth seeking
and increases COX-2 after prolonged abstinence from alcohol. To further examine the role
of COX-2 in alcohol drinking, the second study found that adolescent alcohol drinking not
only increased COX-2 after four weeks of alcohol abstinence, but also increased
endothelin-1 (ET-1) and prostaglandin E2 (PGE2) in the dorsal striatum. Furthermore,
adolescent alcohol drinking increased alcohol drinking after abstinence, and this increase
was attenuated by treatment with the COX-2 inhibitor nimesulide during abstinence.
Antagonism of the interaction between PGE2 and its receptor 1 (EP1) also attenuated the
increase in relapse drinking and restored alcohol drinking to the rate of alcohol naïve rats.
Overall, these experiments identified a prostaglandin-mediated mechanism that is a
putative target for the treatment of alcohol relapse following abstinence in individuals with
a history of adolescent alcohol abuse.
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Effects of Rebamipide on Nephrotoxicity Associated With Selected NSAIDs in RatsWood, Robert C., Wyatt, Jarrett E., Bullins, Kenny W., Hanley, Angela V., Hanley, Gregory A., Denham, James W., Panus, Peter C., Harirforoosh, Sam 15 November 2013 (has links)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30 mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40 mg/kg), diclofenac (10 mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury.
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Effects of Rebamipide on Nephrotoxicity Associated With Selected NSAIDs in RatsWood, Robert C., Wyatt, Jarrett E., Bullins, Kenny W., Hanley, Angela V., Hanley, Gregory A., Denham, James W., Panus, Peter C., Harirforoosh, Sam 15 November 2013 (has links)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30 mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40 mg/kg), diclofenac (10 mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury.
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Aspirin Dose Dependently Inhibits the Interleukin-1β-Stimulated Increase in Inducible Nitric Oxide Synthase, Nitric Oxide, and Prostaglandin E<sub>2</sub> Production in Rat Ovarian Dispersates Cultured in VitroCarnovale, David E., Fukuda, Aisaku, Underhill, Derek C., Laffan, John J., Breuel, Kevin F. 18 April 2001 (has links)
Objective: Determine if aspirin inhibits the IL-1β-stimulated expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO), and prostaglandin E2 (PGE2) in rat ovarian dispersates cultured in vitro. Design: Prospective, controlled in vitro study. Setting: Academic research laboratory. Animals: Ovaries collected from immature rats. Intervention(s): Ovaries were collected from immature rats and enzymatically dispersed. Ovarian dispersates were placed into plates containing media alone or media supplemented with IL-1β (100 U/mL) and varying concentrations of aspirin (0, 1, 3, 5 and 10 mM). Ovarian dispersates were cultured in a humidified environment of 5% CO2 in air at 37°C for 24 or 48 hours. Main Outcome Measure(s): Twenty-four- and 48-hour iNOS, nitrite (a stable metabolite of NO), and PGE2 levels were determined from ovarian dispersates cultured in vitro. Result(s): Administration of IL-1β increased nitrite and PGE2 levels over that observed in the control group after culture of ovarian dispersates for 24 and 48 hours. Aspirin dose dependently reduced the IL-1β-stimulated increase in nitrite production from ovarian dispersates after culture for 24 and 48 hours. Aspirin completely (24 hours) or dose dependently (48 hours) prevented the IL-β-stimulated increase in PGE2. Coadministration of IL-1β and aspirin (10 mM) attenuates IL-1β-stimulated iNOS expression after culture for 24 and 48 hours. Conclusion(s): Aspirin significantly inhibits the IL-1β-stimulated expression of iNOS, NO, and PGE2 in ovarian dispersates cultured in vitro.
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Charakterisierung der Prostaglandin E\(_2\)-Transporte im proximalen Tubulus der Niere im ischämischen akuten Nierenversagen der Ratte unter Einfluss der Gabe von Nebivolol und Metoprolol Tartrat / Characterization of prostaglandine E\(_2\)- transports in proximal tubule of the kidney in acute ischemic renal failure of rats under influence of nebivolol and metoprolol tartrat administrationHeck, Sigrun January 2020 (has links) (PDF)
In dieser Studie wurde untersucht, ob die durch Ischämie (45min clamping) induzierte Herunterregulation der Sekretion organischer Anionen, wie postuliert, zu einer verminderten Ausscheidung von PGE2 führt und wie sich die Relation zu Inulin und PAH-Clearance verhält. Es wurde weiterhin untersucht, ob die Medikation mit Nebivolol (2,5mg, 5mg und 10 mg) oder Metoprolol Tartrat (47,5mg) einen positiven Effekt auf das renale Outcome, unter Berücksichtigung des Einflusses auf die PGE2- Ausscheidung, hat.
PGE2 wird im Akuten Nierenversagen vermehrt gebildet und die Sekretion vermindert, dies führt zu einer verstärkten inflammatorischen Situation, aber im Gegenzug auch zu einer verbesserten renalen mikrovaskuläre Blutversorgung.
Es wurde bei SD-Ratten eine renale Ischämie, durch Abklemmen der Arteriae renales, für 45 min operativ herbeigeführt. Die Gabe der Betablocker erfolgte nach 35min Ischämie. Nach 24h wurden Inulin- und PAH-Clearance gemessen. Die Messung der PGE2- Konzentration in Serum und Urin erfolgte mittels kompetitivem ELISA.
Generell ist ein besseres renales Outcome bei den mit Nebivolol und Metoprolol Tartrat behandelten Tieren zu erkennen. Besonders ausgeprägt war dieser Effekt bei der Gruppe Cl-Nb2,5mg-Gruppe zu erkennen. Unter den Clamping-Gruppen war ebenfalls die PGE2-Claerance bei Clamp-Nb2,5mg am höchsten. Eine Korrelation zwischen erhöhter Inulinkonzentration im Urin (besseres outcome) und erhöhter PGE2- Konzentration im Urin konnte nicht nachgewiesen werden. / This study examined whether the postulated downregulation of OATs (organic anion transporters) in renal ischemic situation reduces a secretion of PGE2 and how this is related to inulin- and pah-clearance. In addition, it was analyzed if medication with the betablockers nebivolol and metoprolol tartrat has a positive effect on the renal outcome, regarding the influence on PGE2-secretion.
The production of PGE2 increases in acute renal failure and its secretion is reduced, which on the one hand intensifies the inflammatory situation in the kidney, but on the other hand improves the microvascular blood support.
SD-rats were subjected to bilateral renal ischemia (45min). After 35min nebivolol (2,5mg, 5mg and 10mg) or metoprolol (47,5mg) were administered. After 24h inulin- and pah-clearance were determined. PGE2 was measured in urine and serum by competitive ELISA.
In general, animals receiving medication had better outcomes. This effect could be observed in the group treated with 2,5 mg nebivolol in particular. Regarding all clamp-groups, the PGE2-clearance was determined the maximum in the clamp2,5mg-group. A correlation between increased inulin-level in urine (better outcome) and increased PGE2-level in urine could not be proved.
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The dissection of the molecular mechanism underlying the facilitative action of prostaglandin E receptor EP1 on dopamine D1 receptor-induced cAMP production / ドパミンD1受容体によるcAMP産生におけるプロスタグランジンE受容体EP1の促進的作用を担う分子機構の解明Aliza Toby Ehrlich 24 September 2013 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(生命科学) / 甲第17931号 / 生博第294号 / 新制||生||38(附属図書館) / 30751 / 京都大学大学院生命科学研究科高次生命科学専攻 / (主査)教授 垣塚 彰, 教授 渡邉 大, 教授 松崎 文雄 / 学位規則第4条第1項該当 / Doctor of Philosophy in Life Sciences / Kyoto University / DFAM
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Roles of Prostaglandin EP4 Receptor in Adipocytes / 脂肪細胞におけるプロスタグランジンEP4受容体の機能解析Inazumi, Tomoaki 24 March 2014 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(薬学) / 甲第18212号 / 薬博第802号 / 新制||薬||237(附属図書館) / 31070 / 京都大学大学院薬学研究科生命薬科学専攻 / (主査)教授 中山 和久, 教授 竹島 浩, 教授 根岸 学 / 学位規則第4条第1項該当 / Doctor of Pharmaceutical Sciences / Kyoto University / DFAM
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Exacerbation of Intracranial Aneurysm and Aortic Dissection in Hypertensive Rat Treated With the Prostaglandin F-Receptor Antagonist AS604872 / プロスタグランジンF受容体選択的阻害薬AS604872は高血圧ラットにおいて脳動脈瘤と大動脈解離を増悪させるFukuda, Miyuki 25 January 2016 (has links)
京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第19397号 / 医博第4048号 / 新制||医||1012(附属図書館) / 32422 / 京都大学大学院医学研究科医学専攻 / (主査)教授 渡邊 直樹, 教授 小泉 昭夫, 教授 木村 剛 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Antiluteogenic effects of serial prostaglandin F2alpha administration in maresCoffman, Elizabeth Ann January 2013 (has links)
No description available.
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