The physiology and pharmacology of nociception from uterine and cervical stimulation has not been well defined but prostaglandins, requiring the cyclo-oxygenase enzyme for synthesis, are likely to play a significant role.
This has the potential to increase nociceptive transduction and NSAIDs may not be as effective in the presence of exogenously supplied prostaglandin, because the cyclo-oxygenase enzyme inhibited is not responsible for the prostaglandin concentration in this setting.
Aspirin produces irreversible inhibition of COX; the synthesis of prostaglandins becomes dependent on the production of new
cyclo-oxygenase enzyme.
Inhibition of the
cyclo-oxygenase enzyme is not selective and there will be decreased production of the positive, anti-inflammatory, 1-series prostaglandins (PGs) as well as the 2-series, pro-inflammatory, ARA metabolites.
Evidence suggests that there may be a synergistic relationship between AVP receptors and
cyclo-oxygenase enzyme during antipyresis, and the presence of AVP may enhance the efficacy of nonsteroidal antipyretic drugs.
This molecule is transformed into PGs via the
cyclo-oxygenase enzyme pathway.
(1992) had earlier found that specific inhibitors of the
cyclo-oxygenase enzyme (i.e., aspirin and indomethacin) seriously repressed ascosporogenesis in the genus Dipodascopsis.
The tripterpenoid cucurbitacin E is also present in watermelon, which provides anti-inflammatory support by blocking activity of
cyclo-oxygenase enzymes which normally lead to increased inflammatory support.