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 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.
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.