PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LICORICE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1991

[Phenolic constituents of licorice. IV. Correlation of phenolic constituents and licorice specimens from various sources, and inhibitory effects of licorice extracts on xanthine oxidase and monoamine oxidase].

The roots and/or rhizomes of Glychyrrhiza uralensis, G. glabra and G. inflata, and commercial licorice specimens from various regions or countries were analyzed by high-performance liquid chromatography (HPLC), and classified into three types based on their phenolic constituents. i) Type A: The roots and rhizomes of G. uralensis, commercial licorice specimens from northwestern region of China (Seihoku-kanzo) and from northeastern region of China (Tohoku-kanzo) in Japanese markets, and also several licorice specimens from Chinese markets. They contain licopyranocoumarin (6), glycycoumarin (7) and/or licocoumarone (8), which were not found in G. glabra and G. inflata. ii) Type B: The root and rhizome of G. glabra, and the licorice specimens imported from the Soviet Union and Afghanistan. They contain glabridin (9) and glabrene (10), which were not found in the samples of the other two Glycyrrhiza species. A root sample of Glycyrrhiza species from Turkey also contains 9 and 10. iii) Type C: The root sample of G. inflata. They contain licochalcones A (11) and B (12), which were not found in the samples of the other two Glycyrrhiza species. Commercial licorice specimens obtained in Japan, which were imported from Sinkiang of China (Shinkyo-kanzo), and some licorice specimens obtained from Chinese markets, have also been found to contain 11 and 12. The phenolics 6-12, characteristic constituents of types A, B or C, were not found in a specimen of cortex-free licorice from a Japanese market (kawasari-kanzo). Extracts of some licorice specimens of types A and B, and all of the licorice specimens of type C inhibited 40-56% of the xanthine oxidase activity at the concentration of 30 micrograms/ml. Extracts of some licorice specimens of types A and B also showed inhibitory effects on monoamine oxidase (44-64% inhibition, at the concentration of 30 micrograms/ml), which were slightly weaker than that of harmane hydrochloride.

Chromatography, High Pressure Liquid↗
PubMed1999

[Variation of chemical constituents in processed licorice roots: quantitative determination of saponin and flavonoid constituents in bark removed and roasted licorice roots].

As a continuing study of chemical characterization of crude drug processing, we have been analyzing the chemical constituents in licorice roots before and after processing. At first, we analyzed chemical constituents in licorice roots of various origins. Next, we have developed the HPLC analytical method, by which saponins and flavonoids, major constituents in various licorice roots, were determined simultaneously in a quantitative manner. In this paper, by means of the HPLC analytical method, chemical constituents in licorice roots, processed and unprocessed, were determined. It was found that nonglycosidic flavonoid constituents were mostly lost while root bark removing, whereas, in roasted licorice roots, sugar chains in the saponin and glycosidic flavonoid constituents were hydrolyzed stepwise during roasting through hydrothermolysis.

Chromatography, High Pressure Liquid↗
PubMed1989

Phenolic constituents of licorice. II. Structures of licopyranocoumarin, licoarylcoumarin and glisoflavone, and inhibitory effects of licorice phenolics on xanthine oxidase.

An anti-HIV (human immunodeficiency virus) phenolic constituent, licopyranocoumarin (4), and two other new phenolics named licoarylcoumarin (5) and glisoflavone (6) were isolated from Si-pei licorice (a commercial licorice; root and stolon of Glycyrrhiza sp. from the north-western region of China) using droplet countercurrent chromatography and centrifugal partition chromatography, and their structures were assigned based on chemical and spectroscopic data. Kaempferol 3-O-methyl ether (7) and licocoumarone (8) were also isolated from the licorice. The inhibitory effects of ten licorice phenolics on xanthine oxidase were examined. Licochalcone B (1), glycyrrhisoflavone (2), 8 and licochalcone A (19) showed 50% inhibition at the concentration of 1.3-5.6 x 10(-5) M.

Coumarins↗
PubMed1991

Phenolic constituents of licorice. III. Structures of glicoricone and licofuranone, and inhibitory effects of licorice constituents on monoamine oxidase.

Two new phenolic compounds, glicoricone (3) and licofuranone (4), were isolated from a species of licorice brought from the northwestern region of China, and their structures were assigned. Among the twelve licorice constituents examined for the inhibition of monoamine oxidase (MAO), six compounds, 3, 4, genistein (6), licopyranocoumarin (7), licocoumarone (14) and glycyrrhisoflavone (15), inhibited the enzyme with the IC50 (concentration required for 50% inhibition of the enzyme activity) values of 6.0 x 10(-5)-1.4 x 10(-4) M. Glycyrrhizin (1) also inhibited MAO with the IC50 value of 1.6 x 10(-4) M.

Animals↗
PubMed2000

Phenolic constituents of licorice. VIII. Structures of glicophenone and glicoisoflavanone, and effects of licorice phenolics on methicillin-resistant Staphylococcus aureus.

Two new phenolic compounds, glicophenone (1) and glicoisoflavanone (2), were isolated from commercial licorice, and their structures were elucidated on the basis of spectroscopic data. Antibacterial assays of licorice phenolics for Staphylococcus aureus, including four strains of methicillin-resistant S. aureus (MRSA), and also for Escherichia coli K12 and Pseudomonas aeruginosa PAO1, were then examined. Two compounds among them, 8-(gamma,gamma-dimethylallyl)-wighteone (21) and 3'-(gamma,gamma-dimethylallyl)-kievitone (28), showed remarkable antibacterial effects [minimum inhibitory concentrations (MICs), 8 microg/ml on the MRSA strains and methicillin-sensitive S. aureus. Licochalcone A (14), gancaonin G (20), isoangustone A (24), glyasperins C (30) and D (31), glabridin, (32), licoricidin (33), glycycoumarin (34) and licocoumarone (40) showed antibacterial effects on the MRSA strains with MIC values of 16 microg/ml. Effects on the beta-lactam resistance of the MRSA strains were also examined, and licoricidin (33) noticeably decreased the resistance of the MRSA strains against oxacillin, as shown by the reduction in the MICs of oxacillin (lower than 1/128-1/1000 in the presence of 8 microg/ml of 33, and 1/8-1/32 in the presence of 4 microg/ml of 33). Mechanistic study suggested that 33 does not inhibit the formation of penicillin-binding protein 2' (PBP2'), but affects the enzymatic function of PBP2'.

Glycyrrhiza↗
PubMed1997

Application of a licorice root specific protein to a general method for the assay of licorice root components in traditional Chinese medicines.

A new fuzzy immunoassay method generally applied to ten Glycyrrhizae Radix (GR) preparations of four different botanical origins was studied. Four kinds of antisera were elicited in rabbits immunized with GRs of different botanical origins. The presence of the characteristic GR protein (GRP) was shown using Western blot analyses and selected antibody enzyme immunoassay (SAEIA) methods. A GRP was isolated from one of the GR specimens which was selected using SAEIA methods. The isolated GRP was heated to reduce its binding activity to an anti-GR serum. A new fuzzy SAEIA method generally applicable for assay of the extract of the ten GR specimens was developed using heat-treated GRP as the solid-phase antigen. The fuzzy SAEIA method was successfully applied for the detection and quantitative analysis of the GR component contained in traditional Chinese medicines.

Animals↗
PubMed2001

['Licorice hypertension' also caused by licorice tea].

A 41-year-old woman, who presented with (apparent) essential hypertension, was treated with atenolol and candesartan. This treatment, however, was unsuccessful. After the addition of hydrochlorothiazide (HCT) to the combination, she developed hypokalaemia with muscle cramps and weakness. This hypokalaemia persisted for more than 4 weeks after discontinuation of HCT and starting potassium suppletion. As a result of polyuria (> 4000 ml/day) found in a 24-hour urine collection, it was discovered that the patient drank at least 3 litres of liquorice tea a day. She had denied eating liquorice sweets, a well-known cause of hypertension in the Netherlands, but no one had thought of asking her if she drank liquorice tea. Blood pressure and serum potassium normalized about 2 months after she stopped drinking liquorice tea, and medication was withdrawn. In a patient presenting with hypertension and hypokalaemia, who denies eating liquorice sweets, one should consider the consumption of other products containing liquorice such as liquorice tea. In the Netherlands liquorice tea is increasingly popular and has recently become available on a large scale. Therefore more cases such as the one described may be expected in coming years.

Adult↗
PubMed2005

Toxicologic evaluation of licorice extract as a cigarette ingredient.

Licorice extract (block, powder or liquid) may be applied to cigarette tobacco at levels of about 1-4% to enhance and harmonize the flavor characteristics of smoke, improve moisture holding characteristics of tobacco, and act as a surface active agent for ingredient application. Neat material pyrolysis studies, and smoke chemistry and biological activity studies (bacterial mutagenicity, cytotoxicity, micronucleus, and sub-chronic inhalation) with mainstream smoke, or mainstream smoke preparations from cigarettes containing various target levels (1.5-12%) of the licorice extracts were performed to provide data for an assessment of the use of licorice extract as a cigarette tobacco ingredient. At simulated tobacco burning temperatures up to 900 degrees C all forms of neat licorice extract pyrolyzed extensively, yielding small amounts of benzene, toluene, phenol and acetaldehyde with no indication that licorice extracts would transfer intact to mainstream smoke. As a single ingredient added to cigarette tobacco, block licorice extract at a target level of 12.5% increased smoke constituents including selected PAH, arsenic, lead, phenol and formaldehyde (on a TPM basis), while licorice extract powder (target level of 8% tobacco) increased select PAH, phenol and formaldehyde (on a TPM basis). Lower target application levels (including typical application levels) of block, powder or liquid licorice extract did not significantly alter the smoke chemistry profile. Biological tests indicated no relevant difference in the genotoxic or cytotoxic potential of either mainstream smoke (or smoke preparations) from cigarettes with added licorice extracts compared to control cigarettes. In sub-chronic 90-day rat inhalation studies, the mainstream smoke from cigarettes with 12.5% added block and 8% added powder licorice extract contained higher formaldehyde concentrations compared to control cigarette smoke. Female rats in the 12.5% block licorice extract exposure group displayed an increased incidence and severity of epithelial hyperplasia in the nose (level 2), with no relevant respiratory tract changes in the 8% powder licorice extract exposed rats. At the lower licorice extract application levels (1.25-5%), there was no indication of increased formaldehyde concentration in the smoke atmosphere and no relevant changes in respiratory tract tissues. Mineralcorticoid-like effects which have been associated with excess licorice ingestion were not found in any of the smoke inhalation studies. The results of these studies with various forms of licorice extract applied to cigarette tobacco suggest that adding licorice extract to cigarette tobacco at levels of < or =5% does not discernibly alter the smoke chemistry or biological effects normally associated with mainstream cigarette smoke.

Animals↗
PubMed2006

High levels of ochratoxin A in licorice and derived products.

The ochratoxin A (OTA) content of 30 samples of licorice root and derived products (licorice-confectionery, licorice block, and licorice extract) was analyzed by a standard HPLC-fluorescence technique and confirmed by methyl-ester formation. All analyzed samples of licorice and derived products were found to contain ochratoxin A, and some of them showed extremely high concentrations up to 252.8 ng/g of OTA. Highest levels of ochratoxin A were found in dry licorice root, averaging 63.6 ng/g, while mean contents in fresh licorice root were 9.2 ng/g. Licorice-confectionery (sweets) contained 3.8 ng/g of OTA. Ochratoxin A was also abundant in two licorice derivatives, liquid licorice extract (16.0 ng/g) and solid licorice block (39.5 ng/g). The ochratoxin levels found in licorice and derived products are higher than those reported in the literature for other food commodities. The experiments of OTA transfer into the tea beverages showed that almost 5% of the OTA present in dry licorice root is transferred to the corresponding decoction tea, whereas only 1% of OTA remains in infusion tea. The significance of the levels of ochratoxin A in licorice and its derivatives is discussed in the context of existing data on ochratoxin contamination in foods.

Beverages↗
PubMed2006

Neuroprotective effects of roasted licorice, not raw form, on neuronal injury in gerbil hippocampus after transient forebrain ischemia.

AIM: To observe neuroprotective effects of raw and roasted licorice against hypoxia and ischemic damage. METHODS: When elucidating the protective effects of raw and roasted licorice, we analyzed the lactate dehydrogenase (LDH) release using PC12 cells after hypoxia in an in vitro study and after transient forebrain ischemia in an in vivo study on Mongolian gerbils. RESULTS: Raw and roasted licorice significantly reduced LDH release from PC12 cells exposed to an hypoxic chamber for 1 h. In the roasted licorice-treated group, the decrease of LDH release was more pronounced compared to that of the raw licorice-treated group. In roasted licorice-treated animals, approximately 66%-71% of CA1 pyramidal cells in the ischemic hippocampus were stained with cresyl violet compared to the control group. However, in the raw licorice-treated animals, no significant neuroprotection against ischemic damage was shown. In addition, ischemic animals in roasted licorice-treated group maintained the Cu, Zn-superoxide dismutase (SOD1) activity and protein levels compared to the control group, while in raw licorice-treated group SOD1 activity and protein levels were reduced significantly. High pressure liquid chromatography analysis showed that non-polar compounds containing glycyrrhizin-degraded products, such as glycyrrhetinic acid (GA) and glycyrrhetinic acid monoglucuronide (GM), were increased in roasted licorice. CONCLUSION: Roasted licorice had neuroprotective effects against ischemic damage by maintaining the SOD1 levels. In addition, the difference in protective ability between raw and roasted licorice may be associated with non-polar compounds, such as GA and GM.

Animals↗
PubMed1995

Inhibitory effect of isoliquiritin, a compound in licorice root, on angiogenesis in vivo and tube formation in vitro.

A water extract of licorice root inhibits granuloma angiogenesis in adjuvant-induced chronic inflammation (Phytother. Res., 5, 195. 1991). The present study has investigated the effects of licorice-derived compounds on granuloma angiogenesis. Isoliquiritin (0.31-3.1 mg/kg), a licorice-derived flavonoid, inhibited the carmine content of granuloma tissue 50-fold greater than licorice extract. Glyeyrrhizin (20-80 mg/kg), a licorice-derived saponin, inhibited carmine content with a weak potency. The licorice extract (0.01-1 mg/ml) also inhibited tube formation from vascular endothelial cells in a concentration-dependent manner. From the chemical structure-activities of used licorice-derived flavonoids (0.1-100 microM), their potencies for anti-tube formation were in the order isoliquiritigenin > isoliquiritin > liquiritigenin >> isoliquiritin-apioside. Glycyrrhizin (0.1-100 microM) and glycyrrhetinic acid (0.1-10 microM) increased tube formation. A glycyrrhizin (82 micrograms/ml)-induced increase in tube formation was inhibited by isoliquiritin. The combined effect of a mixture of 82 micrograms/ml glycyrrhizin and 4.2 micrograms/ml isoliquiritin, a similar concentration ratio to their yield ratio in the licorice extract, corresponded to the effect of 100 micrograms/ml extract. In conclusion, the anti-angiogenic effect of licorice extract depended on the anti-tube formation effect of isoliquiritin.

Animals↗
PubMed2004

Chemical analysis of raw, dry-roasted, and honey-roasted licorice by capillary electrophoresis.

In herbal medicine, licorice is usually processed using a roasting procedure which might modify the chemical compositions in licorice. To test this hypothesis, licorice root samples were roasted under various conditions (with or without honey) and subsequently extracted by refluxing with 95% ethanol. The analysis of chemical compositions of licorice root extracts was achieved by capillary electrophoresis. The running buffer has been optimized to be 50 mM sodium tetraborate (pH 9.01) containing 5 mM beta-cyclodextrin. Thermal decomposition of glycyrrhizin, which was a major ingredient in licorice, was first studied in detail, indicating the conversion of glycyrrhizin to glycyrrhetinic acid. The licorice extracts were then analyzed to indicate the above thermal conversion did occur in the licorice samples. This finding may shed some light on understanding the differences in the therapeutic values of raw versus roasted licorice in herbal medicine.

Chalcone↗
PubMed1994

Licorice and enzymes other than 11 beta-hydroxysteroid dehydrogenase: an evolutionary perspective.

Licorice has long been known to promote the healing of ulcers. In the 1950s, studies with licorice-derived compounds revealed that the anti-ulcer effects of licorice are due to inhibition of 15-hydroxyprostaglandin dehydrogenase and delta 13-prostaglandin reductase. 15-Hydroxyprostaglandin dehydrogenase converts prostaglandins E2 and F2 alpha to 15-ketoprostaglandins, which are inactive. delta 13-Prostaglandin reductase metabolizes the inactive delta 13-prostaglandin to 13,14-dihydro,15-ketoprostaglandin, which is further metabolized and excreted in urine. Thus, licorice-derived compounds have the effect of raising the local concentration of prostaglandins that promote mucous secretion and cell proliferation in the stomach, leading to healing of ulcers. 11 beta-Hydroxysteroid dehydrogenase, which also is inhibited by licorice-derived compounds, shares a common ancestor with 15-hydroxyprostaglandin dehydrogenase. Both enzymes are homologous to Streptomyces hydrogenans 3 alpha,20 beta-hydroxysteroid dehydrogenase, which also is inhibited by licorice. Thus, licorice inhibits enzymes that diverged at least 2 billion years ago from a common ancestor. Other oxidoreductases in bacteria, plants, and animals that are inhibited by licorice-derived compounds are likely to be discovered in the future.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1978

Licorice raises urinary cortisol in man.

The finding that urine cortisol excretion was increased in patients with hypokalaemic hypertension induced by licorice addiction led to this study on the effect of licorice in normal subjects. Thirteen normal volunteers ate either 100 or 200 g licorice for 1-4 weeks and assessment of pituitary-adrenal function was made before, during, and 1 week after cessation of licorice ingestion. Urine cortisol excretion more than doubled in 10 of 13 subjects (mean, 33.8 +/- 15.6 SD before and 83.3 +/- 56 SD micrograms/24 h at 1 week after commencing licorice) and excretion rates similar to those observed in Cushing's syndrome were seen in 7 subjects (range, 91-226, compared to normal range of 11-82 micrograms/24 h). Urine cortisol excretion remained significantly elevated (P less than 0.01) above control levels for at least 1 week after licorice was withdrawn. Despite these increases, urinary steroid metabolite (tetrahydrocortisol, tetrahydrocortisone, tetrahydro-11-deoxycortisol, 17-ketogenicsteroids, and 17-ketosteroids) excretion was not affected, plasma cortisol and ACTH values were unchanged, and normal 0800-1600-h diurnal variation of plasma cortisol was maintained. The direct intraadrenal infusion of the active mineralocorticoid component of licorice, glycyrrhetinic acid, in two sheep with autotransplanted adrenal glands failed to stimulate cortisol secretion acutely. It is concluded from these studies that the licorice-induced changes in cortisol excretion are not a result of adrenocoritcal stimulation but more likely represent a change in the renal handling of cortisol.

Adenoma↗