Anti-inflammatory and analgesic effects have been revealed in several pharmacological studies of extracts of Hp and of compounds isolated from Hp [1, 14]. These studies were carried out over the years using in vivo and in vitro models for antiinflammatory or analgesic drug screening. More recently, studies of Hp extracts and constituent compounds have been performed with the aim of establishing the molecular targets within the network of cytokines, intracellular signal pathways and effector molecules that promote or mediate inflammation. The various pharmacological investigations of Hp are reviewed here. They generally support the notion that Hp extracts exert anti-inflammatory effects and provide some plausible insight into the possible mode of action of Devil's Claw as an anti-inflammatory drug.
There are a number of important caveats due to the design of these studies that hinder interpretation of the data with respect to the medicinal use of Hp. Firstly, the test extract or harpagoside is generally applied before induction of the inflammatory challenge, which is a standard pharmacological paradigm. But this does not reflect the therapeutic paradigm of application to the pre-existing challenged or pathophysiological state. Exceptions were two early negative studies [15,16] in which Hp was administered orally at very high doses to animals with established inflammation and no effect was observed. Frequently, the effect of parenteral administration of the test drug is investigated whereas Hp preparations are usually for oral use. Most of the models involved acute and severe inflammation and short-term treatment, whereas Hp has therapeutic potential in chronic, and frequently mild inflammatory, conditions. The majority of the studies demonstrated anti-inflammatory effects, but used doses of Hp are much higher than doses traditionally used in humans. Despite these caveats, the pharmacological studies described are worth consideration since they provide some important information. The efficacy of very high doses in acute severe inflammatory models can have the corollary of efficacy at lower doses in chronic mild inflammation.
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