Inhibition of arachidonic acid induced

Hall, E.D. and Travis, M.A. (1988) Inhibition of arachidonic acid-induced vasogenic brain edema by the non-glucocorticoid 21-aminosteroid U74006F, Brain Res. 451, 350-352. 

Some inhibition of arachidonic acid-induced platelet aggregation in guinea pig and rat plasma was observed after treatment with Oswego tea essential oil (Tognolini et al. 2006). 

In human plasma, the compound eugenol strongly inhibited platelet aggregation induced by platelet-activating factor. A weaker inhibition was observed on platelet aggregation induced by arachidonic acid or collagen (Saeed et al. 1995). Inhibition of arachidonic acid-induced platelet inhibition was also observed in rabbit plasma (Laekeman et al. 1990). 

The compound curcumin exhibited significant antiplatelet activity in vitro, causing inhibition of arachidonic acid-, collagen- and ADP-induced platelet aggregation with IC50 values of 13.8, 22.4, and 16.8 pM, respectively (Jantan et al. 2007). Inhibition of arachidonate-induced platelet aggregation was observed in human blood platelets treated with turmeric extract (Srivastava 1989). In a similar study, curcumin... 

Meier, R.W., Niklaus, G., Dewald, B., Fey, M.F., and Tobler, A. (1995) Inhibition of Arachidonic Acid Pathway Prevents Induction of IL-8 mRNA by Phorbol Ester and Changes the Release of IL-8 from HL 60 Cells Differential Inhibition of Induced Expression of IL-8, TNF-a, IL-a and IL-ip, 7. Cell Physiol. 165,62 70. 

These steioids aie capable of preventing or suppressing the development of the sweUing, redness, local heat, and tenderness which characterize inflammation. They inhibit not only the acute symptoms of the inflammatory process, such as edema, fibrin deposition, and capillary dilatation, but also the chronic manifestations. There is evidence that glucocorticoids induce the synthesis of a protein that inhibits phosphoHpase A 2 (60), diminishing the release of arachidonic acid from phosphoHpids (Fig. 2), thereby reducing chemotaxis and inflammation. 

Barbour, B Szatkowski, M., Ingledew, N., and Attwell, D. (1989) Arachidonic acid induces a prolonged inhibition of glutamate uptake into glial cells. Nature 342,918-920. 

Pharmacological approaches include the inhibition of release of arachidonic acid by inhibition of phospholipase A2 and the inhibition of acylcarnitine transferase I by and oxfenicine, the latter of which has been shown to prevent or at least delay ischemia-induced uncoupling. There are at present no data available on the possible effects of inhibitors of arachidonic acid release on ischemia-induced uncoupling. 

Flunixin is registered or is under development in many countries for use in horses, cattle, and swine for treatment of equine colic, musculoskeletal disorders, acute endotoxin-induced mastitis in cattle, and respiratory disease (89-91). It is administered orally or parenterally for a maximum of 5 successive days (92). Flunixin is a genotoxic but not carcinogenic compound. Its mechanism of action is believed to be via the inhibition of cycloxygenase to reduce the presence of arachidonic acid metabolites produced during inflammation (93). 

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