Novel contraceptive targets to inhibit ovulation: the prostaglandin E2 pathway.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, preclinical animal (macaque), and human literature
PubMed 26025453 · doi:10.1093/humupd/dmv026
What was done
This narrative review synthesized literature published between 1987 and 2014 examining the prostaglandin E2 (PGE2) synthesis-metabolism-transport pathway during ovulation. It evaluated mechanistic studies in primary ovarian cells and cell lines, in vivo ovulation and breeding experiments in macaques, and human case reports and clinical studies evaluating cyclooxygenase/PTGS2 (COX-2) inhibitors for ovulation suppression.
What was found
The abstract reports no numerical data or statistical effect sizes. Qualitatively, LH triggers follicular expression of PGE2 synthesis, transport, and metabolic machinery. PTGS2 inhibitors reduced ovulation rates in women and decreased cumulus expansion, oocyte release, follicle rupture, oocyte maturation, and fertilization in macaques. In breeding macaques, PTGS2 inhibition reduced pregnancy rates when given as emergency contraception, but failed to prevent pregnancy when administered to simulate monthly contraceptive use.
Why it matters
It defines the PGE2 pathway as a potential non-hormonal target for contraception, demonstrating that while single PTGS2 inhibitors may have utility for emergency contraception, multi-target disruption across PGE2 synthesis, transport, and metabolism is likely required for regular monthly contraception.
Limits
The review is narrative rather than systematic, with no reported search strategy, study counts, or meta-analytic estimates. The abstract reports no quantitative effect sizes. Key contraceptive efficacy findings rely largely on non-human primate models, and monotherapy was ineffective for routine monthly contraception.
Cited by
- supports Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or naproxen around the time of ovulation can inhibit the acute inflammatory cascade and prevent the ovarian follicle from rupturing.