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Results for “Glycyrrhetinic Acid”

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At least 19 recordsLinked to original sources
PubMed2002

[Quantitative determinations of glycyrrhizic acid, glycyrrhetinic acid, morphine and sodium benzoate in compound liquorice tablets by capillary zone electrophoresis].

Capillary zone electrophoresis (CZE) was used to quantitatively determine the contents of glycyrrhizic acid, glycyrrhetinic acid, morphine and sodium benzoate in compound liquorice tablets. The detection wavelength was 228 nm and the applied voltage was 14 kV. Borax solution of 50 mmol/L was used as the background electrolyte and hydrochlorothiazide as the internal standard. There were all good linear relationships between the concentrations and the relative areas of glycyrrhizic acid, glycyrrhetinic acid, morphine and sodium benzoate. Their average recoveries were 98.2%, 97.3%, 97.1% and 97.5%, respectively. The method is simple, rapid and accurate.

Antitussive Agents↗
PubMed2004

On the mechanism of mitochondrial permeability transition induction by glycyrrhetinic acid.

Glycyrrhetinic acid (GE), the aglycone of glycyrrhizic acid, a triterpene glycoside which represents one of the main constituents of licorice root, induces an oxidative stress in liver mitochondria responsible for the induction of membrane permeability transition. In fact, GE, by interacting with the mitochondrial respiratory chain, generates hydrogen peroxide which in turn oxidizes critical thiol groups and endogenous pyridine nucleotides leading to the opening of the transition pore. Most likely the reactive group of GE is the carbonyl oxygen in C-11 which, by interacting mainly with a Fe/S centre of mitochondrial complex I, generates an oxygen-centered radical responsible for the pro-oxidant action.

Animals↗
PubMed1994

Analysis and pharmacokinetics of glycyrrhizic acid and glycyrrhetinic acid in humans and experimental animals.

Glycyrrhizic acid (GZA) and glycyrrhetinic acid (GRA) can be determined rapidly and precisely by high-performance liquid chromatography (HPLC) in biological fluids and tissues from experimental animals and humans. From plasma and tissues, GZA and GRA are extracted by organic solvents and the extracts can directly be used for HPLC. From bile or urine, extraction and determination of GZA and GRA are more difficult due to interfering endogenous compounds and conjugation of GRA with glucuronides or sulfates. Extraction of GZA and GRA from urine or bile can be performed by ion-pairing followed by extraction with organic solvents or by solid phase extraction. GRA conjugates can be determined by chromatographic separation or by pretreatment with beta-glucuronidase. The pharmacokinetics of GRA and GZA can be described by a biphasic elimination from the central compartment with a dose-dependent second elimination phase. Depending on the dose, the second elimination phase in humans has a half-life of 3.5 hours for GZA and between 10-30 hours for GRA. The major part of both GRA or GZA is eliminated by the bile. While GZA can be eliminated unmetabolized and undergoes enterohepatic cycling, GRA is conjugated to GRA glucuronide or sulfate prior to biliary excretion. Orally administered GZA is almost completely hydrolyzed by intestinal bacteria and reaches the systemic circulation as GRA.

Animals↗
PubMed1996

Increased sodium appetite and thirst in rat induced by the ingredients of liquorice, glycyrrhizic acid and glycyrrhetinic acid.

In the rat, blocking 11 beta-OHSD with the active ingredient of liquorice, glycyrrhizic acid (GZA) or its hydrolytic product, 18 beta-glycyrrhetinic acid (GTA), caused potassium loss, increased water intake and a primary increase in salt appetite that was specific for sodium and not secondary to sodium loss. Intracerebroventricular injection of angiotensin II enhanced the sodium appetite but carbachol did not. The stimulating effects of GZA or GTA on intakes of water and NaCl resembled those caused by the administration of excessive amounts of mineralocorticoid. The results suggest that GZA- or GTA-induced drinking behaviour is mediated by circulating glucocorticoids. After liquorice blockade of 11 beta-OHSD, the peripheral and central mineralocorticoid receptors are no longer protected from glucocorticoid action.

Angiotensin II↗
PubMed1993

Inhibition of rat acute inflammatory paw oedema by dihemiphthalate of glycyrrhetinic acid derivatives: comparison with glycyrrhetinic acid.

The anti-inflammatory profile of dihemiphthalate compounds of glycyrrhetinic acid derivatives in acute rat paw oedema induced by various vasoactive agents was compared with the parent compound. Three dihemiphthalate compounds (the di-sodium salt of 18 beta-olean-12-ene- 3 beta,30-diol di-O-hemiphthalate, 18 beta-olean-9(11),12-dione-3 beta,30-diol di-O-hemiphthalate and olean-11,13(18)-diene-3 beta,30-diol di-O-hemiphthalate), significantly inhibited development of carrageenan-induced rat paw oedema during the first 3 h (ED50 70, 90, and 108 mg kg-1 respectively, p.o.), while glycyrrhetinic acid (ED50, 200 mg kg-1) showed a significant inhibition of paw oedema 3 h after carrageenan treatment. The dihemiphthalate compounds also suppressed mouse paw oedema induced by histamine, bradykinin, and PAF acether at doses of less than 100 mg kg-1. However, these compounds failed to inhibit 5-HT-induced mouse paw oedema. Glycyrrhetinic acid had little effect on mouse paw inflammation induced by the above irritants. The three compounds at 10(-7)-10(-4) M, inhibited histamine-induced contraction of guinea-pig isolated ileum. However, concentration-response curves to 5-HT and bradykinin were not affected by the same compounds. These results suggest that the dihemiphthalate compounds modulate vascular permeability caused by endogenous vasoactive agents as one of the anti-inflammatory mechanisms. This action is quite different from that of glycyrrhetinic acid.

Animals↗
PubMed1999

[Determination of chlorogenic acid, glycyrrhizin and glycyrrhetinic acid in yinqiaojiedupian by high performance capillary electrophoresis].

A simple, rapid and reproducible capillary electrophoretic method was developed for the determination of chlorogenic acid, glycyrrhizin and glycyrrhetinic acid in Yinqiaojiedupian. The buffer solution used in this method was a mixture of 20 mmol/L NaH2PO4 and 5 mmol/L Na2B4O7(pH 7.0). The other conditions were as follows: applied voltage, 20 kV (positive to negative polarity); L = 60 cm; Leff = 55 cm; i.d. = 75 microns; lambda = 254 nm; temperature, 25 degrees C; injection time, 5 s hydrostatic. The linear calibration range was 1.568-100.4 mg/L for glycyrrhetinic acid, 8.000-128.0 mg/L for glycyrrhizin and 8.080-129.3 mg/L for chlorogenic acid, and recoveries were 98.0%-103% for glycyrrhetinic acid, 97.3%-102% for glycyrrhizin and 97.3%-100% for chlorogenic acid. The relative standard deviations (n = 3) were 0.2%-1.3% (intra-day) and 1.9%-3.0% (inter-day) for glycyrrhetinic acid, 0.5%-1.2%(intra-day) and 1.9%-2.1%(inter-day) for glycyrrhizin and 0.7%-1.3%(intra-day) and 1.6%-2.1%(inter-day) for chlorogenic acid. The contents of these three acids in Yinqiaojiedupian were successfully determined within 10 min.

Anti-Infective Agents↗
PubMed1991

High-performance liquid chromatographic determination of 18 alpha-glycyrrhetinic acid and 18 beta-glycyrrhetinic acid in rat plasma: application to pharmacokinetic study.

A high-performance liquid chromatographic method for the separation and determination of 18 alpha-glycyrrhetinic acid and 18 beta-glycyrrhetinic acid has been developed. Indomethacin was used as an internal standard. The drugs were separated on a reversed-phase column and detected by UV detection at a wavelength of 254 nm. Methanol-water-perchloric acid-ammonia (80:20:0.4:0.4, v/v) was used as the mobile phase at pH of 7.0-7.5. The detection limit of both compounds was 0.1 microgram/ml in rat plasma. The method was applied to pharmacokinetic studies of glycyrrhetinic acids in rats. The results suggest that the pharmacokinetics appeared to be non-linear in nature.

Ammonia↗
PubMed1996

Evidence that disruption of connexon particle arrangements in gap junction plaques is associated with inhibition of gap junctional communication by a glycyrrhetinic acid derivative.

Glycyrrhetinic acid exhibits many pharmacological activities, including the ability to block gap junctional communication. However, the mechanism of glycyrrhetinic action is not clear. Others have shown that glycyrrhetinic acid apparently binds to a single proteinatious binding site in the plasma membrane. We present evidence that while exposure to glycyrrhetinic acid derivatives may not affect protein synthesis or location, it does seem to alter connexon particle packing in gap junction plaques.

Animals↗
PubMed1993

Inhibition of mutagenicity in Salmonella typhimurium by Glycyrrhiza glabra extract, glycyrrhizinic acid, 18 alpha- and 18 beta-glycyrrhetinic acids.

The effects of Glycyrrhiza glabra L. extract, glycyrrhizinic acid, 18 alpha- and 18 beta-glycyrrhetinic acids on the mutagenicity of the ethyl methanesulfonate, N-methyl-N'-nitro-N-nitrosoguanidine, and ribose-lysine Maillard model systems were investigated by using the Salmonella/microsome reversion assay. The protocol used allowed us to detect desmutagenic and antimutagenic activity and to avoid false positive results due to toxicity. For all the compounds tested, no desmutagenic activity was observed against ethyl methanesulfonate and N-methyl-N'-nitro-N-nitrosoguanidine; only Glycyrrhiza glabra extract showed antimutagenic activity against ethyl methanesulfonate. On using the ribose-lysine mutagenic browning mixture, the desmutagenic activities of the Glycyrrhiza glabra extract, glycyrrhizinic acid, 18 alpha- and 18 beta-glycyrrhetinic acids were observed. 18 beta-Glycyrrhetinic acid was the most active compound. Glycyrrhiza glabra extract also exhibited antimutagenic activity against ribose-lysine.

Antimutagenic Agents↗
PubMed1997

Determination of 18 beta-glycyrrhetinic acid in human serum using the fully automated ALCA-system.

We report a method for the determination of 18 beta-glycyrrhetinic acid (glycyrrhetinic acid) in human serum using the ALCA-system. The technology of the ALCA-system is based on the principles of adsorptive and desorptive processes between liquid and solid phases. The assay is run fully automated and selective. Procedural losses throughout the analysis are negligible, thereby allowing for external calibration. The calibration curve is linear up to 10 mg/l and concentrations as low as 10 micrograms/l are detectable. CV is 2.5% for within- and 7.5% for between-assay precision at a level of 50 micrograms/l and 1.2% for within- and 8.5% for between-assay precision at a level of 500 micrograms/l. Specific and expensive reagents are not necessary and time-consuming manual operations are not involved. This assay can be selected from a wide spectrum of methods at any time. Thus, the present method is well-suited for drug monitoring purposes in the routine laboratory. In a pharmacokinetic study we measured serum levels of glycyrrhetinic acid in ten healthy young volunteers after ingestion of 500 mg glycyrrhetinic acid. Maximum levels of glycyrrhetinic acid were 6.3 mg/l 2 to 4 hours after ingestion. Twenty-four (24) hours after ingestion seven probands still had glycyrrhetinic acid levels above the detection limit with a mean level of 0.33 mg/l.

Adult↗
PubMed1998

Determination of glycyrrhizic acid and 18-beta-glycyrrhetinic acid in biological fluids by micellar electrokinetic chromatography.

A micellar electrokinetic chromatographic technique for determining acid (GZA) and 18 beta-glycyrrhetinic acid (GRA) in human plasma and urine was developed. Sample clean-up and analyte concentration were carried out by solid-phase extraction (with C18 sorbent). The buffer solution used for MEKC contained 20 mM sodium dihydrogenphosphate, 20 mM sodium tetraborate, 20 mM tetrabutylammonium bromide and 50 mM sodium dodecylsulphate, at a pH of 8.7. Good linearities for both GZA and GRA in plasma and urine were obtained. The recoveries of the method were in the range 86.5 to 107%. The detection limits for GZA in urine (0.5 ml) and plasma (1 ml) were 1.6 micrograms ml-1 and 0.8 micrograms ml-1, respectively, while for GRA in urine (0.5 ml) and plasma (1 ml) were 2 micrograms ml-1 and 1 micrograms ml-1, respectively.

Buffers↗
PubMed1991

Specific binding of glycyrrhetinic acid to the rat liver membrane.

Glycyrrhetinic acid bound specifically to a particulate fraction of rat liver. The binding was dependent on time, temperature and pH, equilibrium being reached after 10 min at 37 degrees C. The equilibrium dissociation constant and the maximal concentration of the binding site, as determined by Scatchard plot analysis, were 31 nM and 43 pmol/mg protein, respectively, indicating a single binding site entity. The binding site was highly specific for glycyrrhetinic acid, glycyrrhizin, various steroids, various fatty acids and retinoids showing no or only very low affinity. The binding was inhibited by boiling or treatment with trypsin or phospholipases. The specific activity of glycyrrhetinic acid binding was the highest in the liver, followed by in the kidney. The results suggest that glycyrrhetinic acid plays a significant role in the rat liver through its specific binding protein.

Animals↗
PubMed1996

Anti-inflammatory and anti-nociceptive activity of disodium glycyrrhetinic acid hemiphthalate.

The anti-inflammatory and anti-nociceptive effects of disodium glycyrrhetinic acid hemiphthalate (glycyrrhetinic acid 3 beta-O-hemiphthalate sodium) after parenteral administration were determined in several animal models. Disodium glycyrrhetinic acid hemiphthalate (GAP) significantly inhibited the rat paw edema induced by carrageenin (ID50 = 21.37 mg/kg), and mice writhing responses caused by acetic acid (ID50 = 9.12 mg/kg). The potency of disodium glycyrrhetinic acid hemiphthalate was about 13.05 times higher than acetylsalicylic acid in inhibiting rat paw edema and 12.84 times higher in inhibiting abdominal constrictions in mice.

Analgesics↗
PubMed1975

Binding of glycyrrhetinic acid to kidney mineralocorticoid and glucocorticoid receptors.

Whether the mineralocorticoid effect of glycyrrhetinic acid is mediated by the adrenal glands or is due to a direct action on the renal tubule remains controversial. The affinity of glycyrrhetinic acid for mineralocorticoid receptors has been studied by several types of competition experiments. When rat kidney slices were incubated with 2 times 10- minus 9 M [3H]aldosterone, glycyrrhetinic acid (2 times 10- minus 5 M) was able to compete with aldosterone for the cytosolic receptor and to decrease the formation of a chromatin-[3Hi1 aldosterone-receptor complex. In cytosol, in vitro, 6 times 10- minus 4 M glycyrrhetinic acid was able to inhibit aldosterone binding by 70 percent, whereas the same dose produced only a 20 percent inhibition of dexamethasone binding. The apparent KDiss of glycyrrhetinic acid for the mineralocorticoid receptor was 2 times 10- minus 6 M. That glycyrrhetinic acid appeared to compete mainly with mineralocorticoid receptors was confirmed by sedimentation in the sucrose gradients: [3H]Aldosterone specifically bound to an 8 S peak was displaced by 5 times 10- minus 5 M glycyrrhetinic acid, whereas the [3H]dexamethasone peak was not affected by this compound. Glycyrrhizic acid showed no significant affinity for mineralocorticoid or glucocorticoid kidney receptor sites. Glycyrrhetinic acid and glycyrrhizic acid had no affinity for rat cortisol binding globulin. Glycyrrhetinic acid has a low but definite affinity for mineralocorticoid receptors and thus appears to have a direct mineralocorticoid action. The low affinity of this compound for mineralocorticoid receptors is in good agreement with the very high doses required to exhibit its biological activity.

Aldosterone↗
PubMed2006

Microbial transformation of glycyrrhetinic acid by Mucor polymorphosporus.

Glycyrrhetinic acid (GA; 1) is one of the major constituents of a traditional Chinese medicine, the roots of Glycyrrhiza uralensis, called Gancao in Chinese. In the present paper, the biotransformation of GA by Mucor polymorphosporus (AS 3.3443) was investigated and eight metabolites were obtained. Based on their chemical and spectral data, the structures of the derivatives were respectively elucidated as 24-hydroxyglycyrrhetinic acid ( 2), 6beta-hydroxyglycyrrhetinic acid ( 3), 7alpha-hydroxyglycyrrhetinic acid ( 4), 7beta-hydroxyglycyrrhetinic acid ( 5), 3- O-acetyl-7beta-hydroxyglycyrrhetinic acid ( 6), 3-oxo-7beta-hydroxyglycyrrhetinic acid ( 7), 15alpha-hydroxyglycyrrhetinic acid ( 8), 3 -oxo -15alpha-hydroxyglycyrrhetinic acid ( 9), among which metabolites 3, 4, 6, 7 and 9 are new compounds.

Biotransformation↗
PubMed1994

[Effect of glycyrrhetinic acid on DNA damage and unscheduled DNA synthesis induced by benzo (a) pyrene].

Glycyrrhetinic acid (GA) is an active component of Glycyrrhiza uralensis Fisch. In this study, the effects of glycyrrhetinic acid on DNA damage and unscheduled DNA synthesis induced by benzo (alpha) pyrene were studied. Mouse ear edema was visible obviously at the 6th h after topical application of single dose croton oil. A topical application of croton oil on the back of ICR mice for 5 h, induced elevation of ornithine decarboxylase (ODC) activity in epidermal. The administration of glycyrrhetinic acid (50-200 mg.kg-1.d-1) to animals for 3 days exhibited 20%-80% inhibition of epidermal ornithine decarboxylase activity in a dose-dependent manner. Benzo (alpha) pyrene obviously caused DNA damage and unscheduled DNA synthesis mediated by S9 fraction in Chinese hamster lung cell line. Glycyrrhetinic acid was found to protect the rapid DNA damage induced by benzo (alpha) pyrene. At concentration of 5 micrograms.ml-1, glycyrrhetinic acid exhibited 70% protection. At 20 micrograms.ml-1, this action was more potent and approached to 80%. The addition of hydroxyurea 10 mmol.L-1 suppressed DNA replicative synthesis to 84.04% and benzo (alpha) pyrene stimulated the DNA repair synthesis (6-fold). Glycyrrhetinic acid (20 micrograms.ml-1 and 50 micrograms.ml-1 significantly decreased the stimulation of DNA repair synthesis induced by benzo (alpha) pyrene. This suggests that glycyrrhetinic acid has effective anti-initiating and anti-promoting activities and could be used for cancer chemopreventive purpose.

Animals↗