The pathophysiology of septic shock is complex, involving multiple endogenous mediators as cytokines, nitric oxide (NO), and cycloxygenase
, lipoxygenase and other enzyme systems (reductases, hydroxylases, dehydrogenases) are essential sources of [O.sub.2][sup.*-] and other reactive oxygen species [24,25].
If the inflammatory response is not blocked at this level by exogenous corticosteroids, then continuing activity of phospholipase A2 results in more and more arachidonic acid being produced to start an inflammatory cascade involving cycloxygenase
COX-1 and COX-2 enzymes.
According to the company, clinical trial and epidemiological data of several cycloxygenase
(COX) inhibitors in long-term treatment showed an increased cardiovascular (CV) risks such as thrombotic events, myocardial infarction, and stroke, which can be fatal.
There is evidence indicating that embryo biopsy could exert detrimental effects on embryo quality and development (31) through cell damage and inflammatory response induced by formation of cycloxygenase
and lipoxygenase metabolites such as prostaglandins (PGF2a) (32-34).
The AA is a substrate for cycloxygenase
(COX), which converts it to prostaglandin [G.sub.2] and [H.sub.2].
inhibitors and the antiplatelet effects of aspirin.
The exact mechanisms of action of these products is not clear but TNF, interferon-[gamma], interleukins 10 and 12, cycloxygenase
2 and possibly the pro-inflammatory transcription factor nuclear factor [kappa] B (NF-[kappa]B) are all affected.
For example, [O.sub.3] can trigger the neutral receptors of the airway by inducing lipid peroxidation and the production of cycloxygenase
(Hazucha et al.
According to the company, Inflama-Rest intercepts four pathways that ca n lead to joint discomfort by inhibiting excess production of cycloxygenase
enzyme 2 (COX-2), nitric oxide synthase (iNOS), nuclear factor kappa B (NF-kappa-B) and cytokines.
Prostaglandins are generated from arachidonic acid via the cycloxygenase