Several In vivo studies have Identified anti-Inflammatory and antinociceptive activity for feverfew extracts and parthenollde. When feverfew extracts were orally administered, or pure parthenollde was Injected IP, significant dose-dependent anti-Inflammatory and antinociceptive effects were observed In animal models (Jain & Kulkarnl 1999). Similarly, when feverfew extracts and parthenollde from Tanacetum vulgarewas administered orally In a rat model, gastric ulcer Index was significantly reduced (Tournler et al 1999).
The mechanisms responsible for these effects are not well elucidated. Jain and Kulkarnl (1999) demonstrated that the antinociceptive effect was not mediated through the opiate pathway and was not associated with sedation. In regards to the anti-Inflammatory effect, several mechanisms appear to be responsible.
Two In vitro studies have found evidence of COX and lipoxygenase Inhibition (Capasso 1986, Pugh & Sambo 1988), while other tests reveal no effect on COX (Collier et al 1980, Makheja & Bailey 1982). Inhibition of phosphollpase A2 has also been suggested (Heptlnstall 1988). Direct binding and Inhibition of l-kappa B kinase beta, an Important subunlt Involved In cytoklne-medlated signalling, has been demonstrated for parthenollde In test tube studies (Kwok et al 2001). Parthenollde also Inhibits NO production, an Important regulator and Inducer of various Inflammatory states (Wong & Menendez 1999). More recently, results from an In vivo study confirm that parthenollde Inhibits proinflammatory cytokine responses, although the authors propose that proinflammatory mediators Including chemoklnes (MIP-2), plasma enzyme mediators (complement, kinin and clotting systems) and lipid mediators (COX, PG, platelet-activating factor) are also likely to be Involved (Smollnskl & Pestka 2003).
The essential oil constituent of feverfew, chrysanthenyl acetate, Inhibits PG synthetase In vitro and also seems to possess analgesic properties (Pugh & Sambo 1988).
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