What is 18β Glycyrrhetinic acid?

Glycyrrhetinic acid is a pentacyclic triterpenoid acquired of the beta-amyrin blazon acquired from the hydrolysis of glycyrrhizic acid, which was acquired from the assemble liquorice. It is acclimated in additive and it masks the absinthian aftertaste of drugs like aloe and quinine. It is able in the analysis of comestible abscess and aswell has expectorant (antitussive) properties. It has some added pharmacological backdrop including antiviral, antifungal, antiprotozoal, and antibacterial activities.
Glycyrrhetinic acid inhibits the enzymes (15-hydroxyprostaglandin dehydrogenase and delta-13-prostaglandin) that metabolize the prostaglandins PGE-2 and PGF-2α to their corresponding 15-keto-13,14-dihydro metabolites which are inactive. This causes an added akin of prostaglandins in the digestive system. Prostaglandins arrest belly beard but activate pancreatic beard and close beard in the belly and clearly access abdominal motility. They aswell could could cause corpuscle admeasurement in the stomach. The aftereffect on belly acerbic secretion, advance of close beard and corpuscle admeasurement shows why licorice has abeyant in alleviative comestible ulcer.
PGF-2α stimulates activity of the uterus during abundance and can could could cause abortion, therefore, licorice should not be taken during pregnancy.
The anatomy of glycyrrhetinic acerbic is agnate to that of cortisone. Both molecules are collapsed and agnate at position 3 and 11. This ability be the base for licorice's anti-inflammatory action.
3-β-D-(monoglucuronyl)-18-β-glycyrrhetinic acid, a metabolite of glycyrrhetinic acid, inhibits the about-face of alive cortisol to abeyant cortisone in the kidneys. This occurs via inhibition of the agitator by inhibiting the agitator 11-β-hydroxysteroid dehydrogenase. As a result, cortisol levels are top aural the accession aqueduct of the kidney. Cortisol has built-in mineralocorticoid backdrop (that is, it acts like aldosterone and increases sodium reabsorption) that plan on ENaC channels in the accession duct. Hypertension develops due to this apparatus of sodium retention. People generally accept top claret burden with a low renin and low aldosterone claret level. The added amounts of cortisol binds to the unprotected, ambiguous mineralocorticoid receptors and abet sodium and aqueous retention, hypokalaemia, top claret burden and inhibition of the renin-angiotensin-aldosterone system. Accordingly licorice should not be accustomed to patients with a accepted history of hypertension.
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