These remedies are however less powerful than modern drugs and are most useful as adjuncts to the therapeutic measures listed above.
Feverfew (Tanacetum parthenium )
Ash ( fraxinus excelsior) moderate anti-inflammatory containing coumarin that inhibit T-cells and prostaglandin biosynthesis.
Devil's claw ( Harpagophytum procumbens)
Lignum vitae (Guaiacum spp.)
Bogbean (Menyanthes trifoliate )
Popular bark (Populus spp )containing salicylates with established anti-inflammatory properties.
Willow bark (Salix spp) the original source of salicylates and with strong traditional reputation as an anti-rheumatic.
Feverfew extract (50 or 150 µl/ml) has been shown to suppress 86 to 88% of prostaglandin production without an effect on cyclo-oxygenase. Furthermore, lactones (parthenolide and epoxyartemorin) isolated from feverfew have been found to be inhibitory with IC50 values ranging from approximately 1 to 5 mcg/ml, irreversibly inhibiting eicosanoid generation.
The anti-inflammatory effects of feverfew may be caused by a cytotoxic effect. Feverfew extracts were found to inhibit mitogen-induced tritiated thymidine uptake by human peripheral blood mononuclear cells, interleukin-2-induced tritiated thymidine uptake by lymphoblasts, and prostaglandin release by interleukin-1-stimulated synovial cells. Parthenolide also blocked tritiated thymidine uptake by mitogen-induced human peripheral blood mononuclear cells.
Tanetin, a lipophilic flavonoid found in the leaf, flower, and seed of feverfew, blocks prostaglandin synthesis. Aqueous extracts do not contribute to feverfew's anti-inflammatory activity, but do prevent the release of arachidonic acid and inhibit in vitro aggregation of platelets stimulated by adenosine 5″-diphosphate (ADP) or thrombin. Whether or not these extracts block the synthesis of thromboxane, a prostaglandin involved in platelet aggregation, is controversial. Results suggest that feverfew's inhibition of prostaglandin synthesis differs in mechanism from that of the salicylates.[–]
Feverfew action does not appear to be limited to a single mechanism. Plant extracts affect a wide variety of physiologic pathways. Some of these mechanisms have been discussed previously, including inhibition of prostaglandin synthesis, decrease of vascular smooth muscle spasm, and blockage of platelet granule secretion.
Feverfew appears to be an inhibitor of prostaglandin synthesis. Extracts of the above ground portions of the plant suppress prostaglandin production; leaf extracts inhibit prostaglandin production to a lesser extent. Neither the whole plant nor leaf extracts inhibit cyclooxygenation of arachidonic acid, the first step in prostaglandin synthesis. Chloroform leaf extracts, rich in sesquiterpene lactones, inhibit production of inflammatory prostaglandins in rat and human leukocytes. Inhibition was irreversible and the effect was not caused by cytotoxicity. Studies have shown that lipophilic compounds other than parthenolide may be associated with anti-inflammatory activity, particularly with reducing human neutrophil oxidative burst activity.[,,]