The anti-inflammatory action of GA is largely mediated by Cortisol, an endogenous hormone with anti-inflammatory action (Teelucksingh et al 1990). Several studies have found that GA inhibits the activity of 11 HSD and hepatic delta-4-5-beta-steroid reductase, preventing the conversion of Cortisol to its inactive metabolite, cortisone (Kageyama et al 1997, MacKenzie et al 1990, Soma et al 1994, Whorwood et al 1993). As such, Cortisol activity is prolonged and levels may rise, thereby increasing its anti-inflammatory effects.

For this reason licorice has also been investigated for its ability to potentiate the effects of steroid medications (Teelucksingh et al 1990).

This mechanism alone does not fully account for the anti-inflammatory effects of licorice as oral doses of GL also appear to exert an effect in adrenalectomised rats (Gujral et al 2000). The DGL also exerts anti-inflammatory effects. Steroid-like activity has also been attributed to the liquiritin constituent (Bradley 1992) and in vitro studies of G. inflata reveal that the licochalcone flavonoids A and B inhibit the formation of leukotrienes B4 and C4, cyto-B-induced lysosomal enzyme, platelet-activating factor, N-formyl-methionyl-leucyl-phenylalanine and calcium ionophore A (Kimura et al 1993a). The anti-inflammatory response may also be enhanced by inhibition of the generation of reactive oxygen by neutrophils (Akamatsu et al 1991).

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