There is good in vitro and in vivo pharmacological evidence of the anti-inflammatory and analgesic properties of devil's claw, although some negative findings have also Devil's claw 351
been reported (McGregor et al 2005). Overall, greatest activity appears to be in semi-chronic rather than acute conditions.
Devil's claw exerted significant analgesic effects against thermally and chemically induced nociceptive pain stimuli in mice and significant dose-related reduction of experimentally induced acute inflammation in rats (Mahomed & Ojewole 2004), as well as reducing pain and inflammation in Freund's adjuvant-induced arthritis in rats (Andersen etal 2004).
The iridoids, particularly harpagoside, are thought to be the main active constituents responsible for the anti-inflammatory activity, although the mechanism of action is unknown and devil's claw is also rich in water-soluble antioxidants (Betancor-Fernandez et al 2003).
It has been suggested that the suppression of matrix metalloproteinases in chondrocytes via the inhibition of inflammatory cytokine synthesis, demonstrated in vitro, could explain its therapeutic effect in arthritic inflammation (Kundu et al 2005). In vitro evidence also suggests that the anti-inflammatory effect may be due to effects on TNF-alpha (Fiebich et al 2001) or antioxidant activity (Langmead et al 2002). Additionally, inhibition of leukotriene synthesis has been observed in vitro, which appears to relate to the amount of harpagoside present (Loew et al 2001).
Contradictory evidence exists as to whether devil's claw affects prostaglandin (PG) synthesis. Early in vitro and in vivo studies suggest that it does not inhibit PG synthesis (Whitehouse et al 1983) and this is supported by studies of PG production in humans (Moussard et al 1992). However, more recent investigations have suggested that its anti-inflammatory and analgesic activities are due to suppression of PGE2 synthesis and nitric oxide production and that the herb may suppress expressions of COX-2 and iNOS (Jang et al 2003). More recently, methanoloic extracts of devil's claw have been shown to inhibit COX-2 in vivo (Kundu et al 2005, Na et al 2004).
In vivo experiments have determined that the method of administration of devil's claw affects its anti-inflammatory properties. Intraperitoneal and intraduodenal administration was shown to reduce carrageenan-induced oedema, whereas oral administration had no effect, suggesting that exposure to stomach acid may reduce its anti-inflammatory activity (Soulimani et al 1994). This is supported by a study that found a loss of anti-inflammatory activity after acid treatment (Bone & Walker 1997).
In vitro studies on rat mesangial cells suggest that devil's claw may be used as an anti-inflammatory agent in the treatment of glomerular inflammatory diseases (Kaszkin et al 2004a). Devils claw extract produced a concentration-dependent suppression of nitrite formation in rat mesangial cells in vitro due to an inhibition of Devil's claw 352
iNOS expression through interference with the transcriptional activation of iNOS. It
was found that this activity was due to harpagoside, together with other constituents that possibly have strong anti-oxidant activity (Kaszkin et al 2004b).
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