Deglycyrrhizinated licorice, or DGL, has been used clinically for decades, primarily for the treatment of peptic ulcers. Licorice has many triterpenoids and hundreds of flavonoids that have been shown to inhibit several inflammatory enzymes, including both cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX). These enzymes decrease the production of several potent inflammatory compounds, including IL-6, prostaglandin E2, thromboxane B2, and leukotriene B4. Importantly, this inhibition is not primarily due to glycyrrhizic acid, the component of licorice that has been removed in DGL and that is associated with mineralocorticoid excess and hypertension. Licorice has multiple active compounds with anti-inflammatory, anti-microbial, and anti-allergic actions, including glabridin and at least seven licochalcones. The compounds have been shown to prevent lipopolysaccharide (LPS) induced production of inflammatory compounds, inhibit yeast and bacterial biofilm formation, and upregulate antioxidant enzymes.

Clinically, DGL has been shown to have comparable efficacy to cimetidine for both the healing and prevention of ulcer recurrences. Additionally, extracts of licorice have been shown to inhibit the adhesion of H. pylori to gastric mucosa, as well as the growth of antibiotic resistant strains, suggesting multiple mechanisms of action for its anti-ulcer benefit. The use of chewable tablets appears necessary for DGL’s efficacy as it allows for distribution and absorption by the gastric mucosa.