Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LICORICE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2001

Isolation and identification of main constituents in an enzymatically hydrolysed licorice extract sweetener.

Licorice extract including glycyrrhizin as the major component is used as a safe sweetener in many countries. Enzymatically hydrolysed licorice extract (EHLE) is also used as a sweetener in Japan. In the present paper, the constituents of EHLE were investigated as a part of the studies for evaluating its quality and safety as a food additive. Three oleanane-type monoglycosides along with glycyrrhizin (1) eand 3-O-[beta-D-glucuronopyranosyl-(1-->2)-beta-D-glucuronopyranosyl]-18beta-liquiritic acid (2) were isolated from EHLE. The structures of the three compounds have been determined to be 3-O-beta-D-glucuronopyranosyl-24-hydroxy-18beta-glycyrrhetinic acid (3), 3-O-beta-D-glucur-onopyranosyl-18beta-glycyrrhetinic acid (4) and 3-O-beta-D-glucuronopyranosyl-18beta-liquiritic acid (5) based on MS and NMR. Compound 4 was the monoglycosylated derivactive of glycyrrhizin (1). Compounds 3 amd 5 are the monoglycosylated derivatives of the minor constituents in licorice extract. They were first isolated from EHLE, and compound 5 was a new compound.

Glucuronidase↗
PubMed2003

The treatment of atopic dermatitis with licorice gel.

Glycyrrhiza glabra L. has been used in herbal medicine for skin eruptions, including dermatitis, eczema, pruritus and cysts. The effect of licorice extract as topical preparation was evaluated on atopic dermatitis. The plant was collected and extracted by percolation with suitable solvent. The extract was standardized, based on Glycyrrhizinic acid by using a titrimetry method. Different topical gels were formulated by using different co-solvents. After standardizing of topical preparations, the best formulations (1% and 2%) were studied in a double-blind clinical trial in comparison with base gel on atopic dermatitis over two weeks (30 patients in each group). Propylene glycol was the best co-solvent for the extract and Carbopol 940 as gelling agent showed the best results in final formulations. The quantity of glycyrrhizinic acid was determined 20.3% in the extract and 19.6% in the topical preparation. Two percent licorice topical gel was more effective than 1% in reducing the scores for erythema, oedema and itching over two weeks (p<0.05). The results showed that licorice extract could be considered as an effective agent for treatment of atopic dermatitis.

Acrylic Resins↗
PubMed1985

Body-sodium and blood volume in a patient with licorice-induced hypertension.

A 68-year-old man a nine-year history of licorice ingestion had moderate hypertension and low plasma potassium. Exchangeable sodium and blood volume were increased to 128 and 111%, respectively of the expected values; plasma renin and aldosterone levels were suppressed. Plasma norepinephrine concentration was distinctly elevated but the pressor response to infused norepinephrine was normal. After licorice withdrawal, blood pressure, plasma potassium and blood volume reverted to normal levels within three weeks, exchangeable sodium and plasma renin within four months. Exchangeable sodium in our patient with licorice-induced hypertension was increased to a comparable extent as in primary hyperaldosteronism. Moreover, blood pressure in relation to body sodium or plasma potassium did not differ between the exogenous or the endogenous types of mineralocorticoid excess. This observation does not support the possibility that in primary hyperaldosteronism excess aldosterone secretion per se could play an important pressor role independently from sodium retention.

Aged↗
PubMed1989

Effects of licorice on plasma atrial natriuretic peptide in healthy volunteers.

Ingestion of licorice, 100 g daily for 8 weeks, caused a rise in 81% in plasma atrial natriuretic peptide (ANP) concentration in 12 healthy subjects. Mean body weight increment (1.6 kg) correlated with the increase in plasma ANP (r = 0.59; P less than 0.01). The plasma concentrations of antidiuretic hormone, aldosterone, and plasma renin activity decreased. All these hormonal effects, reflecting retention of sodium and fluid volume, were probably due to the known mineralocorticoid properties of licorice. Blood pressure increased transiently and two subjects developed reversible hypertension. The rise in plasma ANP concentration during ingestion of licorice may be considered a physiological response to prevent fluid retention and development of hypertension.

Adult↗
PubMed2002

The licorice root derived isoflavan glabridin inhibits the activities of human cytochrome P450S 3A4, 2B6, and 2C9.

The potent antioxidants licorice root extract and glabridin, an isoflavan purified from licorice root extract, were tested for their ability to modulate the activities of several cytochrome P450 (P450) enzymes. P450 3A4, the major human drug metabolizing P450 enzyme, was inactivated by licorice root extract and by glabridin in a time-and concentration-dependent manner. The inactivation was NADPH-dependent and was not reversible by extensive dialysis. Further analysis showed that the loss in enzymatic activity correlated with a loss in the P450-reduced CO spectrum and with a loss of the intact heme moiety. In contrast, incubations of P450 3A4 with similar concentrations of 2,4-dimethylglabridin and NADPH did not lead to inactivation of P450 3A4. P450 2B6 was also inactivated by glabridin in a time- and concentration-dependent manner. The majority of the glabridin-inactivated P450 2B6 was able to form a reduced CO spectrum suggesting that the heme was not modified with this isoform. High-performance liquid chromatography analysis of the P450 heme confirmed that incubations with glabridin and NADPH did not result in the destruction of the heme moiety. The activity of P450 2C9 was competitively inhibited by glabridin, whereas P450 2D6 and P450 2E1 were virtually unaffected. The data show that glabridin can serve as a substrate for at least three human P450 enzymes and that depending on the isoform, metabolism of glabridin can lead to mechanism-based inactivation or inhibition of the P450. Heme and reduced CO spectral analysis also indicated that glabridin inactivated P450s 2B6 and 3A4 by different mechanisms.

Aryl Hydrocarbon Hydroxylases↗
PubMed2005

Licorice: a possible anti-inflammatory and anti-ulcer drug.

The purpose of this investigation was to study the anti-inflammatory activities of both glycerrhitinic acid (GA) and the aqueous licorice extract (ALE) in comparison with diclofenac sodium (DS) (10 mg/kg), using the carrageenan-induced paw edema model in male albino rats. In addition, the anti-ulcer activities of ALE, famotidine (FT), and a combination of ALE and FT using indomethacin-induced ulceration technique in rat stomach were investigated. Conventional DS tablets containing GA, as well as DS chewable tablets containing either GA or ALE with different tastes were prepared. Also, rapidly disintegrating FT tablets were prepared using direct compression and camphor sublimation methods. ALE or GA produced significant anti-inflammatory activity similar to DS, and when taken concomitantly, there is no possible antagonism. The anti-ulcer activity of licorice was found to be similar to that of FT in indomethacin-induced ulceration technique in rat stomach. Combination therapy of both FT and licorice showed higher anti-ulcer activity than either of them alone. Generally, tablets containing the crosslinked sodium carboxymethyl cellulose (AcDisol) showed more rapidly disintegrating effect than those including Sodium starch glycolate (Primojel). The oral disintegration was very rapid for all the tested formulations. Also, the amount of FT absorbed from the oral cavity was nearly 9 from 10 mg theoretically present in each formula. It could be concluded that both GA and ALE have anti-inflammatory activity comparable with DS. It may be recommended to add ALE to either FT or diclofinac for more effective anti-inflammatory or anti-ulcer formulations, respectively.

Animals↗
PubMed1993

Licorice inhibits 11 beta-hydroxysteroid dehydrogenase messenger ribonucleic acid levels and potentiates glucocorticoid hormone action.

11 beta-Hydroxysteroid dehydrogenase (11 beta HSD) is responsible for the interconversion of cortisol to cortisone [corticosterone (B) to 11-dehydrocorticosterone in rodents] and confers ligand specificity to the mineralocorticoid receptor. Inhibition of 11 beta HSD by licorice derivatives [glycyrrhizic and glycyrrhetinic (GE) acids] results in cortisol/B and not aldosterone acting as a potent mineralocorticoid. 11 beta HSD is ubiquitously expressed and, by converting active glucocorticoid to inactive metabolites, may be an important prereceptor regulator of ligand access to the glucocorticoid receptor (GR). To investigate this further, we have studied the effect of 11 beta HSD inhibition by licorice derivatives on PRL gene expression (a known glucocorticoid target gene) in rat pituitary GH3 cells. Glycyrrhizic acid administration to rats in vivo (75 mg/kg.day for 5 days) resulted in inhibition of 11 beta HSD activity, as previously reported, but also a significant reduction in steady state 11 beta HSD mRNA levels in both predominantly mineralocorticoid (kidney and distal colon) and glucocorticoid (liver and pituitary) target tissues. In vitro, 11 beta HSD mRNA and activity were present in rat pituitary GH3 cells (81% conversion of B to 11-dehydrocorticosterone/4 x 10(6) cells after 24-h incubation) and inhibited by GE in a dose-dependent fashion. While B or GE alone (10(-8)-10(-5) M) had little or no effect on PRL mRNA levels or immunoassayable PRL, combinations of GE plus B resulted in marked inhibition of PRL mRNA levels and secretion, to such an extent that a concentration of 10(-6) M B with 10(-6) M GE was more potent than equimolar concentration of the synthetic GR agonist RU 28362. This inhibitory effect on PRL mRNA levels was blocked by a 10-fold excess of the GR antagonist RU 38486, but not by a 10-fold excess of the mineralocorticoid receptor antagonist RU 26752, confirming that this potentiation of glucocorticoid hormone action was operating through the GR and not the mineralocorticoid receptor. In addition to its established role as a competitive inhibitor of 11 beta HSD, licorice results in pretranslational inhibition of 11 beta HSD both in vitro and in vivo. 11 beta HSD is clearly an important mechanism in regulating tissue levels of active glucocorticoid and, hence, ligand supply to the GR.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1995

3-Monoglucuronyl-glycyrrhetinic acid is a major metabolite that causes licorice-induced pseudoaldosteronism.

18 beta-Glycyrrhetinic acid (GA) has been thought to be one of the major metabolites that causes licorice-induced pseudoaldosteronism. However, we found no difference in the blood level of GA between the patients with and without pseudoaldosteronism. We measured the blood concentration of 3 beta-D-(monoglucuronyl)18 beta-glycyrrhetinic acid (3MGA), another metabolite of 3 beta-D-diglucuronyl-18 beta-glycyrrhetinic acid (glycyrrhizin), by high performance liquid chromatography and found an increased concentration of 3MGA in 10 patients with licorice-induced pseudoaldosteronism, but not in 11 patients without pseudoaldosteronism. To investigate whether 3MGA can inhibit 11 beta-hydroxysteroid dehydrogenase, we incubated rat renal microsome with or without 3MGA and measured the conversion rate of [3H]cortisol to [3H]cortisone. 3MGA was found to be a potent inhibitor of 11 beta-hydroxysteroid dehydrogenase, allowing cortisol to exert its full mineralocorticoid effects. These results suggest that licorice-induced pseudoaldosteronism is due to an increased concentration of 3MGA, but not GA, in the circulating blood of these patients.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2001

Cloning and characterization of a cDNA encoding beta-amyrin synthase involved in glycyrrhizin and soyasaponin biosyntheses in licorice.

An oxidosqualene cyclase cDNA, termed GgbAS1, was isolated from cultured cells of licorice (Glycyrrhiza glabra) by heterologous hybridization with cDNA of Arabidopsis thaliana LUP1 lupeol synthase. The yeast transformed with an expression vector containing the open reading frame of GgbAS1 produced beta-amyrin, indicating that GgbAS1 encodes beta-amyrin synthase involved in the glycyrrhizin and soyasaponin biosyntheses in licorice. Northern blot analysis showed that the level of beta-amyrin synthase mRNA was drastically changed in the cultured licorice cells, whereas the mRNA level of cycloartenol synthase was relatively constant.

Amino Acid Sequence↗
PubMed2005

Phylogenetic relationship of Glycyrrhiza lepidota, American licorice, in genus Glycyrrhiza based on rbcL sequences and chemical constituents.

Two known saponins, licorice-saponin H2 and macedonoside A, were isolated from the stolons of Glycyrrhiza lepidota (American licorice) as major saponins. Since licorice-saponin H2 and macedonoside A are minor saponins isolated from the three glycyrrhizin-producing species (i.e. G. glabra, G. uralensis, G. inflata) and the three macedonoside C-producing species (i.e. G. macedonica, G. echinata, G. pallidiflora), respectively, the present study suggests that G. lepidota is an intermediate of both glycyrrhizin-producing and macedonoside C-producing species. The phylogenetic tree constructed from the nucleotide sequences of ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit gene (rbcL) of these seven Glycyrrhiza plants indicated that G. lepidota was separated from the other six Glycyrrhiza species, and this phylogenetic relationship was in accordance with their saponin compositions.

Glycyrrhiza↗
PubMed1993

Saponin and sapogenol. XLVIII. On the constituents of the roots of Glycyrrhiza uralensis Fischer from northeastern China. (2). Licorice-saponins D3, E2, F3, G2, H2, J2, and K2.

Following the characterization of licorice-saponins A3 (2), B2 (3), and C2 (4), the chemical structures of licorice-saponins D3 (5), E2 (6), F3 (7), G2 (8), H2 (9), J2 (10), and K2 (11), seven of the ten oleanane-type triterpene oligoglycosides isolated from the air-dried roots of Glycyrrhiza uralensis Fischer collected in the northeastern part of China, were investigated. On the basis of chemical and physicochemical evidence, the structures of licorice-saponins D3, E2, F3, G2, H2, J2, and K2 have been determined to be expressed as 3 beta-[alpha-L-rhamnopyranosyl(1-->2)-beta-D-glucuronopyranosyl(1-- >2)-beta-D-glucuronopyranosyloxy]-22 beta-acetoxyolean-12-en-30-oic acid (5), 3-O-[beta-D-glucuronopyranosyl(1-->2)-beta-D- glucuronopyranosyl]glabrolide (6), 3-O-[alpha-L-rhamnopyranosyl(1-->2)-beta-D-glucuronopyranosyl(1--> 2)-beta-D-glucuronopyranosyl]-11-deoxoglabrolide (7), 24-hydroxyglycyrrhizin (8), 3-O-[beta-D-glucuronopyranosyl(1-->2)-beta- D-glucuronopyranosyl]liquiritic acid (9), 24-hydroxy-11-deoxoglycyrrhizin (10), and 3 beta-[beta-D- glucuronopyranosyl(1-->2)-beta-D-glucuronopyranosyloxy]-24-+ ++hydroxyoleana- 11,13(18)-dien-30-oic acid (11), respectively.

China↗
PubMed1993

Saponin and sapogenol. L. On the constituents of the roots of Glycyrrhiza uralensis Fischer from Xinjiang, China. Chemical structures of licorice-saponin L3 and isoliquiritin apioside.

From the air-dried roots of Glycyrrhiza uralensis Fischer collected in Xinjiang province, China ("Shinkyo-Kanzo" in Japanese), a new oleanene-type triterpene oligoglycoside named licorice-saponin L3 and a new chalcone oligoglycoside named isoliquiritin apioside were isolated together with glycyrrhizin, 18 alpha-glycyrrhizin, apioglycyrrhizin, araboglycyrrhizin, licorice-saponins A3, E2, G2, and H2, and six known flavonoid glycosides. On the basis of chemical and physicochemical evidence, the structures of licorice-saponin L3 and isoliquiritin apioside were elucidated as 3 beta-[alpha-L-rhamnopyranosyl(1-->2)-alpha-L-arabinopyranosyl(1--> 2)-beta-D-glucuronopyranosyloxy]-22 beta-acetoxy-24-hydroxyolean-12-en-30-oic acid (1) and 4-O-[beta-D-apiofuranosyl(1-->2)-beta-D- glucopyranosyl]isoliquiritigenin (6), respectively.

Chalcone↗
PubMed2007

Suppression by licorice flavonoids of abdominal fat accumulation and body weight gain in high-fat diet-induced obese C57BL/6J mice.

We applied licorice flavonoid oil (LFO) to high-fat diet-induced obese C57BL/6J mice and investigated its effect. LFO contains hydrophobic flavonoids obtained from licorice by extraction with ethanol. The oil is a mixture of medium-chain triglycerides, having glabridin, a major flavonoid of licorice, concentrated to 1.2% (w/w). Obese mice were fed on a high-fat diet containing LFO at 0 (control), 0.5%, 1.0%, or 2.0% for 8 weeks. Compared with mice in the control group, those in the 1% and 2% LFO groups efficiently reduced the weight of abdominal white adipose tissues and body weight gain. A histological examination revealed that the adipocytes became smaller and the fatty degenerative state of the hepatocytes was improved in the 2% LFO group. A DNA microarray analysis of the liver showed up-regulation of those genes for beta-oxidation and down-regulation of those for fatty acid synthesis in the 2% LFO group. These findings suggest that LFO prevented and ameliorated diet-induced obesity via the regulation of lipid metabolism-related gene expression in the liver.

Adipocytes, White↗
PubMed2004

Myoclonus and metabolic alkalosis from licorice in antacid.

A 90-year-old woman with hypertension developed metabolic alkalosis and myoclonus. Her medications included diltiazem hydrochloride, benidipine hydrochloride, kallidinogenase, procaterol hydrochloride, sennoside, dihydrocodeine phosphate, and KM powder antacid that contained 354 mg of licorice and 900 mg of sodium bicarbonate per 3.9 g of powder. Endocrinological studies showed slightly reduced plasma renin activity and normal plasma aldosterone concentration. A provisional diagnosis of licorice-induced metabolic alkalosis was established and the patient was successfully treated after correction of serum pH and cessation of the medications. Licorice-induced metabolic alkalosis must be considered in the differential diagnosis of myoclonus.

Aged↗
PubMed2001

[Licorice-induced pseudoaldosteronism in a patient with a non-functioning adrenal tumor].

A 72-year-old man was diagnosed with hypertension, hypokalemia, and left adrenal tumor at another hospital, and was referred to our hospital on suspicion of primary aldosteronism. Investigations revealed low plasma aldosterone concentration, and the left adrenal tumor proved to be nonfunctioning, not hyperfunctioning. "Licorice" had been prescribed for the treatment of recurrent cramps in his calf. After stopping the licorice, his condition changed to normokalemia strongly suggesting that his pseudoaldosteronism had been caused by the drug. We reviewed 140 reports on licorice-induced pseudoaldosteronism in Japan, and found a second patient who might have suffered a similar coincidental nonfunctioning adrenal tumor.

Adrenal Gland Neoplasms↗
PubMed1999

[Comparison of constituents extracted from prepared Licorice by semi-bionic extraction with those by water extraction].

OBJECTIVE: To study the granulation of prepared licorice. METHOD: Semi-bionic extraction(SBE) and water extraction(WE) were used in the extraction of prepared licorice, and then compared with glycyrrhetinic acid, total flavone and extract with which were taken as the indexes. RESULT: SBE is superior to WE. CONCLUSION: It is better to use SBE in the preparation of oral licorice granules.

Drugs, Chinese Herbal↗
PubMedDate not supplied

Comparison of antioxidant activity of extract from roots of licorice (Glycyrrhiza glabra L.) to commercial antioxidants in 2% hydroquinone cream.

Powdered dry roots of licorice (Glycyrrhiza glabra L.) were extracted with methanol. Licorice extract was tested for antioxidative activity in comparison with antioxidants (sodium metabisulfite and BHT) at 0.1%, 0.5%, 1.0%, and 2.0% w/w in 2% w/w hydroquinone cream. The systems were incubated in a dark room at 25 degrees +/- 0.5 degrees C and 45 degrees +/- 0.5 degrees C for three months. The physical stability and the percentages of hydroquinone remaining after two weeks and one, two, and three months were determined by UV spectrophotometer at 294 nm according to official standard procedures. The experiment revealed that oxidation degradation of hydroquinone was accelerated by heat even with the existence of antioxidants. The higher percentages of remaining hydroquinone were observed for higher antioxidant concentration but showed lower physical stability in the formulation in the presence of commercial antioxidants, especially in the cases of 1.0% and 2.0% BHT. In the third month, at 25 degrees +/- 0.5 degrees C and 45 degrees +/- 0.5 degrees C, the extract demonstrated more antioxidant activity from two other commercial antioxidants at all concentrations, with about 43-53% and 34-46%, respectively, more hydroquinone remaining than in the control system (p<0.001). In the third month, the preparation containing 0.1%, 0.5%, 1.0%, and 2.0% extract gave good physical formulation stability with about 72%, 76%, 78%, and 81 % hydroquinone remaining at 25 degrees +/- 0.5 degrees C and 51%, 55%, 60%, and 63% hydroquinone remaining at 45 degrees +/- 0.5 degrees C, respectively. This suggested the possibility of using a licorice extract at 0.5% and 1.0% as an effective natural antioxidant for substances that are oxidation-susceptible.

Antioxidants↗