Naproxen sodium decreases prostaglandins secretion from cultured human endometrial stromal cells modulating metabolizing enzymes mRNA expression

Patrizia Carrarelli, Lucia Funghi, Simone Bruni, Stefano Luisi, Felice Arcuri, Felice Petraglia
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2015 · vol. 32(4) , pp. 319–322 · doi:10.3109/09513590.2015.1115973 · PMID:26634864 · W2191092840
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Naproxen sodium treatment of cultured human endometrial stromal cells reduced PGE2 secretion and COX-2 mRNA expression while increasing HPDG mRNA, suggesting it targets endometrial prostaglandin synthesis.

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Abstract

Dysmenorrhea, defined as painful cramps occurring immediately before or during the menstrual period, is a common symptom of different gynecological diseases. An acute uterine inflammatory response driven by prostaglandins (PGs) is responsible for painful symptoms. Progesterone withdrawal is responsible for activation of cyclooxygenase (COX-2) enzyme and decrease of hydroxyprostaglandin dehydrogenase (HPDG) with consequent increased secretion of PGs secretion, inducing uterine contractility and pain. The most widely used drugs for the treatment of pelvic pain associated with menstrual cycle are non steroidal anti-inflammatory drugs (NSAIDs). The uterine site of action of these drugs is still not defined and the present study evaluated the effect of naproxen sodium in cultured human endometrial stromal cells (HESC) collected from healthy women. PGE2 release was measured by ELISA; COX-2 and HPDG mRNA expression were assessed by qRT-PCR. Naproxen sodium did not affect HESC vitality. Naproxen sodium significantly decreased PGE2 secretion (p < 0.01) and COX-2 mRNA expression (p < 0.01). TNF-α induced PGE2 release was reduced in presence of naproxen sodium (p < 0.05), in association with decreased COX-2 and increased HPDG mRNAs expression. Naproxen sodium decreases endometrial PGE2 release induced by inflammatory stimulus acting on endometrial COX-2 and HPDG expression, suggesting endometrial synthesis of prostaglandins as a possible target for reduction of uterine inflammatory mechanism in dysmenorrhea.

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Condition tags

dysmenorrhea

MeSH descriptors

Anti-Inflammatory Agents, Non-Steroidal Dinoprostone Endometrium Naproxen Adult Anti-Inflammatory Agents, Non-Steroidal Cells, Cultured Cyclooxygenase 2 Cyclooxygenase 2 Dinoprostone Endometrium Endometrium Endometrium Endometrium Female Humans Naproxen Stromal Cells Stromal Cells Stromal Cells

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References (44)

SciLite annotations

chemicals 12
naproxen sodium prostaglandin prostaglandin progesterone naproxen sodium naproxen sodium naproxen sodium prostaglandin
organisms 2
human human

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