Non-steroidal anti-inflammatory drugs (NSAIDs) and ovulation: lessons from morphology.

M. Gaytán, C. Morales, C. Bellido, J. E. Sánchez‐Criado, F. Gaytán
In: Histology and histopathology · 2006 · vol. 21(5) , pp. 541–56 · doi:10.14670/hh-21.541 · PMID:16493584 · W1506695970
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

NSAID treatment disrupts ovulation by inhibiting COX-2 and prostaglandin synthesis, interfering with the spatial targeting of follicle rupture at the apex, a process not fully developed in young rats.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This paper reviews and integrates findings from rat studies examining how non-steroidal anti-inflammatory drugs (NSAIDs), likely through cyclooxygenase-2 (COX-2) inhibition and reduced prostaglandin synthesis, affect ovulation. It reports that cycling rats treated with indomethacin during the preovulatory period show abnormal ovulation characterized by disrupted spatial targeting of follicle rupture at the ovarian apex, and that gonadotropin-primed immature rats also develop age-dependent ovulatory defects resembling those seen with indomethacin. The authors note that while prostaglandins are implicated in ovulation, the molecular targets and precise roles of these mediators in the ovulatory process are not fully understood, and that the spatial mechanisms may be less established in very young rats. Relevance to endometriosis: the paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match related to NSAIDs and reproductive physiology.

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Abstract

Ovulation constitutes the central event in ovarian physiology, and ovulatory disfunction is a relevant cause of female infertility. Non-steroidal anti-inflammatory drugs (NSAIDs), widely used due to their analgesic and anti-inflammatory properties, consistently inhibit ovulation in all mammalian species investigated so far, likely due to the inhibition of cyclooxygenase 2 (COX-2), the inducible isoform of COX, that is the rate-limiting enzyme in prostaglandin (PG) synthesis. COX-2 inhibition has major effects on ovulation, fertilization and implantation, and NSAID therapy is likely implicated in human infertility and could be an important, frequently overlooked, cause of ovulatory disfunction in women. Although there is compelling evidence for a role of PGs in ovulation, the molecular targets and the precise role of these compounds in the ovulatory process are not fully understood. Morphological studies from rats treated with indomethacin (INDO), a potent inhibitor of PG synthesis, provide evidence on the actions of NSAIDs in ovulation, as well as on the possible roles of PGs in the ovulatory process. Cycling rats treated with INDO during the preovulatory period show abnormal ovulation, due to disruption of the spatial targeting of follicle rupture at the apex. Noticeably, gonadotropin-primed immature rats (widely used as a model for the study of ovulation) show age-dependent ovulatory defects similar to those of cycling rats treated with INDO. These data suggest that NSAID treatment disrupts physiological mechanisms underlying spatial targeting of follicle rupture at the apex, which are not fully established in very young rats. We summarize herein the ovulatory defects after pharmacologic COX-2 inhibition, and discuss the possible mechanisms underlying the anti-ovulatory actions of NSAIDs.

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