In Western Medicine Glycyrrihiza is used to mask unpleasant tastes, and as an antitussive and expectorant. After World War II, research on the pharmacology of Glycyrrhiza revealed the electrolytic, ACTH-like property of glycyrrhizin, and its anti-inflammatory and anti-allergic actions. In Japan intravenous injections of glycyrrhizin preparations have been widely used. Initial attention was paid to the glucuronic acid contained in glycyrrhizin. There are records of the detoxication of this acid, later, attention shifted to aglycone. At that time glycyrrhizin was believed to have primarily anti-allergic and detoxicative properties.

Intraperitoneal injection of glycyrrhizin at a low dose into rats caused atrophy of the thymus gland and increased the weight of the adrenal gland suggesting the presence of corticotropin like actions. Most authors believe that glycyrrhetinic acid, whose chemical structure is similar to that of the corticosteroids, is the constiuent which produces the adrenocorticomimetic action.

The extract, powder, glycyrrhizin, and glycyrrhetinic acid of the herb exhibited deoxycorticosterone-like action, reducing the urinary volume and sodium excretion and increasing potassium excretion in various animal species.

The direct mineralocorticoid effect of Glycyrrhiza root is probably due to the affinity of glycyrrhetic acid for kidney aldosterone receptors.

The anti-inflammatory and anti-allergic qualities of glycyrrhizin were not originally known, but were discovered in clinical studies. Through animal experiments both effects were verified, as was glycyrrhizin's anti-ulcerative action.

Compared with cortisol, glycyrrhizin should be used at a 10 times greater strength, but from the similarity of its chemical structure and the actions of its electrolytic hormones, it is regarded as having a similar steroid-like, anti-inflammatory effect.

The herbs antiinflammatory action resembles that of butazone or hydrocortisone. Its antiinflammatory principles were found to be glycyrrhizin and glycyrrhetinic acid.

Experiments to test the antiinflammatory actions included the cotton pellet method, the formalin edema method, and the granuloma puch method in rats: as well as tuberculin reaction in BCG-infected marmots skin (5). Compared with cortisol, glycyrrhizin should be used at a 10 times greater strength, but from the similarity of its chemical structure and the actions of its electrolytic hormones, it is regarded as having a similar steroid-like antiinflammatory effect.

Significant inhibition on experimental ulcers in albino rats, produced by litigation of the pylorus, was obtained from subcutaneous injection or intraduodenal administration of the herb extract at the dose of 250mg/kg. Marked reductions of gastric juice and free acid and total acidity were observed 4 hours after pyloric litigation. Recent studies indicated that cAMP and cGMP could regulate gastric acid secretion and maintain the dynamic equlibrium of gastric acid. Glycyrrhetinic acid intragastrically given at the dose of 300mg/kg to rats did not effect adenyl cyclase of the gastric mucosa but could inhibit phosphodiesterase activity, thereby increasing cAMP level of the mucosae of the pylorus and cardia, and suppressing gastric acid secretion.

It has also been shown that the water extract of Glycyrrhiza can inhibit the secretion of gastric juice and the formation of ulcers in the front stomach of rats, after ligation of the polyrus. It prevented gastric ulcers from forming.

Hepatic Action

The use of Glycyrrhiza in treating chronic hepatitis has been verified and has won high praise.

At concentrations of 5-10g/ml of Fm or Fm 100, antiacetylcholine reactions were obtained. Thus although the ingredients of licorice had no atropine-like properties, they do possess papavarine-like, idosyncratic, and antispasmodic capabitities.

Experiments on mice revealed that the herb extract or glycyrrhizine had significant detoxicant actions against chloral hydrate, strychnine, urethrane, cocaine, arsenobenzene and mercurous chloride. The detoxicant mechanism of the herb has not been wholly elucidated. Some investigators believe that the action of the herb is probably realized through the absorbtive activity of glycyrrhizin the adrenocorticometic action of glycyrrhetinic acid, the glucuronic acid-like conjugation detoxicant action and through the amelioration of the regulative activity of the pituitary-adrenal system.

In patients with mild Addisons disease requiring daily intramuscular injection of 12.5mg of cortisone, the concurrent daily intramuscular injection of glycyrrhizin, starting from the third day after the determination of urinary corticosterone, increased urinary free 17-hydroxycorticosterone and decreased the conjugated 17-hydroxycorticosterone, but did not change the total amount excreted. Except for the tendency of the total 17-hydroxycorticosterone to decrease slightly, similar results were obtained in healthy individuals given intramuscular injections of glycyrrhizin at the dose of 80mg, twice daily. This study suggests that glycyrrhizin can prolong the action of cortisone.

Glycyrrhizin at a concentration of 8mM completely inhibited growth and the cytopathic effects of vaccinia, herpes simplex type 1, Newcastle disease, and vesicular stomatiis viruses in cultures of human aneuploid HEP2 cells. At the same concentration, glycyrrhizin inactivated herpes simplex virus irreversibly. The action mechanism of glycyrrhizin is based on the interaction with sensitive virus proteins at the virionic stage and during a later phase when these proteins are synthesized in host cells.

Glycyrrhizin was found to completely inhibit human immunodeficiency virus-induced plaque formation in MT-4 cells at the concentration of 0.5mg/ml. The ID₅₀ was 0.125mg/ml. It also completely inhibited the human immunodeficiency virus-induced cytoplasmic effect and virus specific antigen expression in MT-4 cells. In comparison to glycyrrhizin, glycyrrhizin sulfate showed a stronger activity against human immunodeficiency virus.

Glycyrrhizin and glycyrrhetic acid were able to prevent the development of experimental cirrhosis. In rats intoxicated with CCl₄, the elevation of serum glutamic oxalacetic transaminase and the accumulation of triglyceride in the liver were decreased. Histopathological studies revealed that liver lesions in rats incuced by CCl₄ were less severe in glycyrrhizin and glycyrretic acid treated animals than in controls. The liver glycogen level in treated rats was markedly decreased.

Except those noted, all references come from Weng Weiliang, et al., Clinical Chinese materia medica, Henan Science & Technology Press, 1998