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

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dc.contributor.authorGaytán, M.es
dc.contributor.authorMorales, C.es
dc.contributor.authorBellido, C.
dc.contributor.authorSánchez-Criado, J.E.
dc.contributor.authorGaytán, F.
dc.date.accessioned2011-06-30T12:02:42Z
dc.date.available2011-06-30T12:02:42Z
dc.date.issued2006
dc.description.abstractOvulation constitutes the central event in ovarian physiology, and ovulatory disfunction is a relevant cause of female infertility. Non-steroidal antiinflammatory 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 ratelimiting 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 posible 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, gonadotropinprimed 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 posible mechanisms underlying the anti-ovulatory actions of NSAIDs.es
dc.formatapplication/pdfes
dc.format.extent16es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/22649
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectIndomethacines
dc.subjectOvulationes
dc.subject.other61 - Medicinaes
dc.titleNon-steroidal anti-inflammatory drugs (NSAIDs) and ovulation, lessons from morphologyes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.21, nº 5 (2006)