Furthermore, proanthocyanidin has also been reported to have anti-carcinogenic, anti-inflammatory, anti-bacterial, anti-viral, cardioprotective, and immune system stimulant properties by inhibiting phospholipase A2, cyclooxygenase, and lipooxygenase
enzymes (22, 23).
The mechanism of action involves inhibition of the cyclooxygenase enzyme, and blockade of the synthesis of prostaglandins (PG), but they have no effect in the lipooxygenase
enzyme activity, responsible for the synthesis of LTs (10, 11), which are the most important inflammatory mediators in gouty arthritis (10).
A study showed that etomidate increases the responsiveness to norepinephrine in an endothelium-dependent way, which is partially independent of the action of nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), cyclooxygenase products, lipooxygenase
products, angiotension-II and Endothelin (15).
modulation to reserve carcinogenesis.
The result of the decrease in arachidonic acid for eicosanoid formation and competition with the n-3 FAs for the cyclooxygenase and lipooxygenase
enzyme sites generally results in decreased production of the 2-series prostanoids, such as thromboxane A2 (TXA2) and prostaglandin E2.
2][alpha] in peritoneal fluids as well as lipooxygenase
products, which stimulate the nociceptive neurons sensitive to NSAIDs (18), (24) Therefore, the results of the acetic acidinduced writhing strongly suggests that the mechanism of this extract may be linked partly to inhibition of lipooxygenase
and/or cyclooxygenase in peripheral tissues, reducing in [PGE.
Other arachidonic metabolites are formed via the lipooxygenase
and cycloxygenase pathways and cause amplification of the inflammatory response and increased vascular permeability.
In addition, Quercetin also inhibits the enzymes cyclooxygenase and Lipooxygenase
which catalyses the conversion of arachidonic acid to its metabolites (42,43,44).
The synthetic estrogen DES is oxidized to DES quinone to yield ROS by hydroperoxidase activity of lipooxygenase
, which might be associated with the toxic effect of this synthetic estrogen (Nunez-Delicado et al.
This may be mediated through cyclooxygenase and lipooxygenase
products of arachidonic acid.
Antiinflammatory activity is related to glucocorticosteroids ability to inhibit phospholipase A2, cyclooxygenase and lipooxygenase
pathways, thereby limiting the release of arachidonic acid and its metabolites.