Fertility and sterility · 2012
Chlormadinone acetate suppresses prostaglandin biosynthesis in human endometrial explants.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hanjalic-Beck Aida, Schäfer Wolfgang R, Deppert Wolfgang R, Fischer Lara, Stein Antonia, Seebacher Laura, von Gradowski Akou Seli, Stuckenschneider Johanna, Zahradnik Hans P
Аннотация
OBJECTIVE: To elucidate the mode of action of chlormadinone acetate (CMA) in reducing dysmenorrheic pain by studying the effects of CMA and dexamethasone (DEX) on messenger RNA (mRNA) abundance of cyclo-oxygenase-2 (COX-2), annexin-1 (ANXA1), glucocorticoid receptor (GR), progesterone receptor (PR), and concentrations of prostaglandin F(2α) (PGF(2α)) and leukotrienes B(4) (LTB(4)) and C(4) (LTC(4)) in human endometrial explants.
DESIGN: Ex vivo study.
SETTING: University hospital.
PATIENT(S): Fifteen premenopausal patients undergoing surgery for benign gynecologic disorders.
INTERVENTION(S): Endometrial explants were obtained by aspiration curettage and stimulated ex vivo with interleukin-1β before exposure to CMA or DEX; mRNA levels were determined via reverse transcription-quantitative real-time polymerase chain reaction, and concentrations of arachidonic acid metabolites by enzyme immunoassays.
MAIN OUTCOME MEASURE(S): Messenger RNA levels of COX-2, ANXA1, PR, and GR; concentrations of PGF(2α), LTB(4), and LTC(4) in endometrial explants treated with CMA or DEX.
RESULT(S): In IL-1β-treated explants COX-2 mRNA and PGF(2α), concentrations were significantly down-regulated by CMA but not by DEX. Chlormadinone acetate did not affect mRNA abundance of ANXA1, PR, and GR.
CONCLUSION(S): Our data suggest that CMA is a suppressor of COX-2 expression. Comparison with DEX revealed that progestin-specific activity of CMA may mainly be responsible for suppression of prostaglandin biosynthesis in human endometrium.
DESIGN: Ex vivo study.
SETTING: University hospital.
PATIENT(S): Fifteen premenopausal patients undergoing surgery for benign gynecologic disorders.
INTERVENTION(S): Endometrial explants were obtained by aspiration curettage and stimulated ex vivo with interleukin-1β before exposure to CMA or DEX; mRNA levels were determined via reverse transcription-quantitative real-time polymerase chain reaction, and concentrations of arachidonic acid metabolites by enzyme immunoassays.
MAIN OUTCOME MEASURE(S): Messenger RNA levels of COX-2, ANXA1, PR, and GR; concentrations of PGF(2α), LTB(4), and LTC(4) in endometrial explants treated with CMA or DEX.
RESULT(S): In IL-1β-treated explants COX-2 mRNA and PGF(2α), concentrations were significantly down-regulated by CMA but not by DEX. Chlormadinone acetate did not affect mRNA abundance of ANXA1, PR, and GR.
CONCLUSION(S): Our data suggest that CMA is a suppressor of COX-2 expression. Comparison with DEX revealed that progestin-specific activity of CMA may mainly be responsible for suppression of prostaglandin biosynthesis in human endometrium.
Предметные рубрики MeSH
AdolescentAdultAnnexin A1Chlormadinone AcetateContraceptives, Oral, SyntheticCyclooxygenase 2DexamethasoneDinoprostDysmenorrheaEndometriumFemaleGlucocorticoidsHumansInterleukin-1betaLeukotriene B4Leukotriene C4Organ Culture TechniquesProstaglandinsRNA, MessengerReceptors, GlucocorticoidReceptors, ProgesteroneYoung Adult