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What is prostaglandin synthesis

T1 - Salicylate reverses in vitro aspirin inhibition of rat platelet and vascular prostaglandin generation

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Aspirin and Prostaglandin Synthesis

Detailed mechanisms depend on the internal structure of COX, which biochemists did not know. They investigated external properties of COX and discovered that it behaves differently in different situations. Some COX enzymes, for instance those in the stomach, are present all the time. Others, for instance those responsible for pain-inducing prostaglandins, appear only at the heel of physiological injuries. This and other experimental results prompted biochemists to speculate that COX existed in two similar but distinct forms.

A history of the science and technology behind aspirin from willow bark to COX inhibitor.

For patients with peripheral arterial occlusive disease stage III or IV not eligible for arterial reconstruction, Prostaglandin E1 (PGE1) therapy not only has significant beneficial effects over placebo on ulcer healing and pain relief but also increases the rate of patients surviving with both legs after 6-months follow-up.
Prostaglandin E1 may be beneficial for some patients with erectile dysfunction.

by inhibiting prostaglandin synthesis.

Nonsteroidal anti-inflammatory medications (NSAIDs) and selective cyclooxygenase-2 (COX-2) inhibitors reduce Prostaglandin E2 production to diminish the inflammation seen in these diseases, but have toxicities that may include both gastrointestinal bleeding and prothrombotic tendencies.

The mechanism of aspirin-hypersensitivity in asthmatic patients is not immunological but is related to pharmaco­logical properties of ASA and other NSAIDs. As originally documented in 1975 by Andrew Szczeklik et al (7), only NSAIDs that are strong or at least moderate inhibitors of prostaglandins (more specifically, inhibitors of COX-1, an enzyme that converts arachidonic acid into prostaglandins, thromboxanes and prostacycline), can cause reactions in ASA-intolerant patients. It is postulated that inhibition of COX-1 by aspirin or other NSAIDs triggers a biochemical cascade which causes asthma. In fact, a local deficiency in prostaglandin E2 synthesis was found in nasal polyps, epithelial cells and bronchial fibroblasts from ASA-hypersensitive patients, suggesting a basal defect in this regulatory mechanism which may be further exacerbated by aspirin (8, 9).

Prostaglandin, role of food, herbs, blockers - Ray Sahelian

It is generally accepted that aspirin inhibits platelet function by irreversible acetylation of prostaglandin cyclo-oxygenase. The salicylate moiety seems not to be causally involved in the inhibitory effect of aspirin, a concept supported by the virtual inactivity of sodium salicylate. However, prostaglandin synthesis is also inhibited by numerous compounds which have no acetylating properties. Recent evidence indicates that salicylate may prevent the inhibitory effect of aspirin on rabbit platelet cyclo-oxygenase, suggesting that interaction of the salicylate moiety of aspirin with this enzyme is important. This study was aimed at evaluating whether the inhibitory effect of aspirin on platelet prostaglandin generation could be reversed by sodium salicylate. We therefore measured spectrophotometrically malondialdehyde (MDA) generated by arachidonate in rat platelet-rich plasma and evaluated the effect of short-term incubation with either aspirin or salicylate or both. In the experimental conditions used, salicylate not only prevented but also reversed aspirin-inhibition of MDA formation. This interaction was not peculiar for platelets, since salicylate also reversed the in vitro inhibitory effect of aspirin on vascular prostacyclin generation (measured by a bioassay). These findings suggest that irreversible acetylation of cyclo-oxygenase does not account for the early in vitro inhibitory effect of aspirin on prostaglandin synthesis.

Arachidonic acid, or AA, is what Series 2 prostaglandins, or the "bad" prostaglandins, are made from.

Series 2 prostaglandins promote platelet aggregation (clot formation); inflammation; sodium retention; and may influence heart disease, blood clots, increased cortisol production, etc..

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  • Ray Peat – Aspirin, Brain and Cancer

    Prostaglandin synthesis;

  • 04/02/2016 · Clinical Implications of Basic Research

    Aspirin - Wikipedia

  • Basic Implications of Clinical Observations

    Prostaglandin influence on health, role of food and diet, (nutrition information) July 1 2017 by Ray Sahelian, M.D

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Boots Aspirin and Codeine Tablets BP - - (eMC)

N2 - It is generally accepted that aspirin inhibits platelet function by irreversible acetylation of prostaglandin cyclo-oxygenase. The salicylate moiety seems not to be causally involved in the inhibitory effect of aspirin, a concept supported by the virtual inactivity of sodium salicylate. However, prostaglandin synthesis is also inhibited by numerous compounds which have no acetylating properties. Recent evidence indicates that salicylate may prevent the inhibitory effect of aspirin on rabbit platelet cyclo-oxygenase, suggesting that interaction of the salicylate moiety of aspirin with this enzyme is important. This study was aimed at evaluating whether the inhibitory effect of aspirin on platelet prostaglandin generation could be reversed by sodium salicylate. We therefore measured spectrophotometrically malondialdehyde (MDA) generated by arachidonate in rat platelet-rich plasma and evaluated the effect of short-term incubation with either aspirin or salicylate or both. In the experimental conditions used, salicylate not only prevented but also reversed aspirin-inhibition of MDA formation. This interaction was not peculiar for platelets, since salicylate also reversed the in vitro inhibitory effect of aspirin on vascular prostacyclin generation (measured by a bioassay). These findings suggest that irreversible acetylation of cyclo-oxygenase does not account for the early in vitro inhibitory effect of aspirin on prostaglandin synthesis.

Boots Aspirin and Codeine Tablets BP - by THE BOOTS COMPANY PLC


We previously showed pomegranate seed oil and fermented juice polyphenols to retard oxidation and prostaglandin synthesis, to inhibit breast cancer cell proliferation and invasion, and to promote breast cancer cell apoptosis.

All mammalian cells except erythrocytes synthesize eicosanoids

AB - It is generally accepted that aspirin inhibits platelet function by irreversible acetylation of prostaglandin cyclo-oxygenase. The salicylate moiety seems not to be causally involved in the inhibitory effect of aspirin, a concept supported by the virtual inactivity of sodium salicylate. However, prostaglandin synthesis is also inhibited by numerous compounds which have no acetylating properties. Recent evidence indicates that salicylate may prevent the inhibitory effect of aspirin on rabbit platelet cyclo-oxygenase, suggesting that interaction of the salicylate moiety of aspirin with this enzyme is important. This study was aimed at evaluating whether the inhibitory effect of aspirin on platelet prostaglandin generation could be reversed by sodium salicylate. We therefore measured spectrophotometrically malondialdehyde (MDA) generated by arachidonate in rat platelet-rich plasma and evaluated the effect of short-term incubation with either aspirin or salicylate or both. In the experimental conditions used, salicylate not only prevented but also reversed aspirin-inhibition of MDA formation. This interaction was not peculiar for platelets, since salicylate also reversed the in vitro inhibitory effect of aspirin on vascular prostacyclin generation (measured by a bioassay). These findings suggest that irreversible acetylation of cyclo-oxygenase does not account for the early in vitro inhibitory effect of aspirin on prostaglandin synthesis.

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