Arachadonic acid metabolites

A study by W. Breu and M. Hagenlocher, published in the German journal Arzneim-Forsch Drug Research in 1992, used a supercritical carbon dioxide extract of saw palmetto. The researchers were exploring the mechanism of action of this herb for benign prostatic hyperplasia. Most research has studied and confirmed the ability of Serenoa to inhibit 5-alpha-reductase and reduce the formation of DHT. The researchers in this experiment found another mechanism of action for saw palmetto inhibition of the biosynthesis of inflammatory arachadonic acid metabolites, specifically the cyclooxygenase and 5-lipoxgenase pathways. 

Inflammatory mediators released at the site of an injury stimulate a cascade of events necessary for the repair and resolution of injury. A number of cells participate in the inflammatory response, including monocytes/ macrophages, neutrophils, and lymphocytes. Structural cells such as fibroblasts and epithelial cells also play critical roles in directing the inflammatory response. Cellular injury results in the release of reactive oxygen species, arachadonic-acid metabolites, inflammatory cytokines, and chemokines that generate an inflammatory response. These paracrine mediators orchestrate complex interactions between the surrounding cell populations and direct the inflammatory responses necessary to restore homeostasis. The chemokine family members appear to play a particularly important role in directing the movement and localization of immune and inflammatory cells. 

Ca + mobilization by metabolites of arachadonic acid. One possible mechanism by which this amplification process could proceed is through Ca + activation of enzymes involved in arachadonic acid (AA) metabolism. In this regard, it is known that blood platelets metabolize endogenous AA to the potent... 

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