HER2 Support Group Forums - View Single Post - NSAIDS consistently inhibit ovulation in all mammalian species investigated so far

R.B. · 05-30-2006, 03:12 PM

I have no idea if this fact might be of potential use in treatment?

What is impact on oestrogen ?

Could it be used with inhibitors etc ?.

The possible use of cox blockers as adjuncts to treatment in BC is an issue that has appeared on several occasions.

It is new and its implications both to those trying to conceive particularly in the field of sports etc and those who may wish to moderate fertiity may be potententially significant.

RB

"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,"

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Histol Histopathol. 2006 May;21(5):541-56. Related Articles, Links
Click here to read
Non-steroidal anti-inflammatory drugs (NSAIDs) and ovulation: lessons from morphology.

Gaytan M, Morales C, Bellido C, Sanchez-Criado JE, Gaytan F.

Department of Cell Biology, Physiology and Immunology, School of Medicine, University of Cordoba, Spain.

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.

Publication Types:

* Review

PMID: 16493584 [PubMed - indexed for MEDLINE]

05-30-2006, 03:12 PM	#1
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	NSAIDS consistently inhibit ovulation in all mammalian species investigated so far I have no idea if this fact might be of potential use in treatment? What is impact on oestrogen ? Could it be used with inhibitors etc ?. The possible use of cox blockers as adjuncts to treatment in BC is an issue that has appeared on several occasions. It is new and its implications both to those trying to conceive particularly in the field of sports etc and those who may wish to moderate fertiity may be potententially significant. RB "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," http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum 1: Histol Histopathol. 2006 May;21(5):541-56. Related Articles, Links Click here to read Non-steroidal anti-inflammatory drugs (NSAIDs) and ovulation: lessons from morphology. Gaytan M, Morales C, Bellido C, Sanchez-Criado JE, Gaytan F. Department of Cell Biology, Physiology and Immunology, School of Medicine, University of Cordoba, Spain. 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. Publication Types: * Review PMID: 16493584 [PubMed - indexed for MEDLINE]