Liquiritigenin, an aglycone of liquiritin in Glycyrrhizae radix, prevents acute liver injuries in rats induced by acetaminophen with or without buthionine sulfoximine

Kim, Young Woo; Ki, Sung Hwan; Lee, Jong Rok; Lee, Song Jin; Kim, Choon Won; Kim, Sang Chan; Kim, Sang Geon

doi:10.1016/j.cbi.2006.03.008

Cited by 108 publications

(78 citation statements)

References 24 publications

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“…ERβ is expressed in brain centers related to learning and memory and is less likely than ERα to be related to sexual function [14,15] . Second, liquiritigenin has been shown in several studies to exert cytoprotective effects [16,17] ; recent studies demonstrate that liquiritigenin exerts anti-inflammatory effects through the NF-κB pathway [18] . Third, we previously observed that liquiritigenin did not induce proliferation of MCF-7 and T47D breast cancer cells (data not shown), which is consistent with other studies [13] .…”

Section: Introductionmentioning

confidence: 99%

Liquiritigenin inhibits Aβ25–35-induced neurotoxicity and secretion of Aβ1–40 in rat hippocampal neurons

2009

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Aim: To examine whether liquiritigenin, a newly found agonist of selective estrogen receptor-β, has neuroprotective activity against β-amyloid peptide (Aβ) in rat hippocampal neurons. Methods: Primary cultures of rat hippocampal neurons were pretreated with liquiritigenin (0.02, 0.2, and 2 μmol/L) prior to Aβ 25-35 exposure. Following treatment, viability of the cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis and by a lactate dehydrogenase activity-based cytotoxicity assay. Intracellular Ca 2+ concentration ([Ca 2+ ] i ) and levels of reactive oxygen species (ROS), as well as apoptotic rates, were determined. Our studies were extended in tests of whether liquiritigenin treatment could inhibit the secretion of Aβ 1-40 as measured using an ELISA method. In order to analyze which genes may be involved, we used a microarray assay to compare gene expression patterns. Finally, the levels of specific proteins related to neurotrophy and neurodenegeration were detected by Western blotting. Results: Pretreated neurons with liquiritigenin in the presence of Aβ 25-35 increased cell viability in a concentration-dependent manner. Liquiritigenin treatment also attenuated Aβ 25-35 -induced increases in [Ca 2+ ] i and ROS level and decreased the apoptotic rate of neurons. Some genes, including B-cell lymphoma/leukemia-2 (Bcl-2), neurotrophin 3 (Ntf-3) and amyloid β (A4) precursor protein-binding, family B, member 1 (Apbb-1) were regulated by liquiritigenin; similar results were shown at the protein level by Western blotting. Conclusion: Our results demonstrate that liquiritigenin exhibits neuroprotective effects against Aβ 25-35 -induced neurotoxicity and that it can decrease the secretion of Aβ 1-40 . Therefore, liquiritigenin may be useful for further study as a prodrug for treatment of Alzheimer's disease.

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Section: Introductionmentioning

confidence: 99%

Liquiritigenin inhibits Aβ25–35-induced neurotoxicity and secretion of Aβ1–40 in rat hippocampal neurons

2009

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“…Liquiritigenin has various beneficial properties such as hepatoprotective [1], anti-cancer [6,7] and anti-inflammatory activity [4]. SIRT1 is a NAD + -dependent protein deacetylase that is involved in the regulation of gene expression, cell metabolism, and differentiation in many organisms including yeast, bacteria, and humans [36].…”

Section: Activation Of Sirt1 Expressionmentioning

confidence: 99%

“…Glycyrrhiza uralensis has been used as traditional and alternative medicine in some countries [1][2][3] because various flavonoids including liquiritin, liquiritigenin, iso-liquiritigenin and other bioactive derivatives have tremendous pharmacological functions. It was found that liquiritin exist mainly as glucoside form of bioactive compound [4,5], while liquiritigenin, an aglycone of liquiritin is present in small amounts in G. uralensis [1].…”

Section: Introductionmentioning

confidence: 99%

“…It was found that liquiritin exist mainly as glucoside form of bioactive compound [4,5], while liquiritigenin, an aglycone of liquiritin is present in small amounts in G. uralensis [1]. There are several studies on their beneficial effects including prevention of carcinogenesis [6,7], hepatoprotective effects [1], and anti-inflammatory effects [4].…”

Section: Introductionmentioning

confidence: 99%

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Production of Liquiritigenin with Cell-based Biotransformation and Its Anti-Aging Activity

Hwang¹,

Jeong²,

Park

2015

KSBB Journal

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In this study, an efficient whole cell-based biotransformation for the production of liquiritigenin was developed using Laetiporus sulphureus CS0218 as biocatalyst and aqueous extracts of Glycyrrhiza uralensis as co-substrate, respectively. In order to determine the efficacy of this method, the optimal bioconversion conditions including mycelial growth, three important enzyme activities (β-glucosidase, α-rhamnosidase and β-xylosidase), and apparent viscosity of culture broth were monitored. After optimization, aqueous extracts of G. uralensis were added to the culture medium to directly produce algycone liquiritigenin. By applying this strategy, 67.5% of liquiritin was converted to liquiritigenin at pH 3.0 after 9 days of incubation and finally liquiritigenin was purified from the reaction mixture. And then, their biological activities including anti-oxidant and superoxide dismutase were observed. In fact, purified liquiritigenin was capable of bi-directional functions (i.e., either up-regulation or down-regulation of SIRT1 which is associated with aging). The results indicate that this strategy would be beneficial to produce biologically active liquiritigenin and could be used in pharmaceutical, cosmetic and food applications.

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“…Our previous studies demonstrated the hepatoprotective effects of LQ against endotoxins and xenobiotics in vivo and in vitro. [23][24][25] In the present study, we investigated the effects of LQ against tacrine-induced cell death and oxidative stress in rats and hepatocyte-derived cell lines, and the underlying mechanisms involved.…”

mentioning

confidence: 99%

Tacrine, an Oral Acetylcholinesterase Inhibitor, Induced Hepatic Oxidative Damage, Which Was Blocked by Liquiritigenin through GSK3-beta Inhibition

Park

Han

et al. 2015

Biological & Pharmaceutical Bulletin

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Although the cholinesterase inhibitor tacrine has been successfully used for the treatment of Alzheimer's disease, it is known to have hepatotoxic effects. Liquiritigenin (LQ), an active flavonoid in Glycyrrhizae radix, exerts protective effects against liver damage. This study investigated the toxic effect of tacrine on hepatocytes and the beneficial effect of LQ on tacrine intoxication in vivo and in vitro, and the underlying mechanism involved. In hepatocyte cell lines, tacrine induced cell death and oxidative stress, as indicated by decreases in cell viability and glutathione (GSH) contents, which were blocked by pretreatment with LQ. Fluorescent activated cell sorter (FACS) analysis revealed that LQ inhibited cellular H 2 O 2 production and mitochondrial dysfunction induced by tacrine in HepG2 cells. Furthermore, LQ promoted inhibitory phosphorylation of glycogen synthase kinase-3β (GSK3β) and prevented decreases in GSK3β phosphorylation induced by tacrine. In rats treatment with tacrine at 30 mg/kg increased hepatic damage as assessed by blood biochemistry and histopathology. Administration of LQ (10 or 30 mg/kg/d, per os (p.o.)) or the hepatoprotective drug sylimarin (100 mg/kg/d) for 3 d inhibited elevations in alanine aminotransferase, aspartate aminotransferase, and histological changes induced by tacrine. These results show that LQ efficaciously protects the rat liver against tacrine-induced liver damage, and suggest that LQ is a therapeutic candidate for ameliorating the hepatotoxic effects of tacrine.Key words tacrine; liquiritigenin; glycogen synthase kinase-3β; liver; oxidative stress; mitochondria Tacrine (9-amino-1,2,3,4-tetrahydroacridine hydrochloride) is recommended as the first-line treatment for Alzheimer's disease by the US Food and Drug Administration. It is an active cholinesterase inhibitor that blocks the degradation of cholinergic nerves in the cerebral cortex and hippocampus to increase cholinergic transmission. 1) However, although tacrine has positive therapeutic effects, it has been demonstrated to increased serum alanine aminotransferase (ALT) levels in about 30% of patients, and this seriously limits its clinical use.2) A number of authors have reported that tacrine-induced hepatotoxicity is related to cytochrome P450 1A2 in human liver microsomes and is associated with mitochondrial dysfunction.3-5) Studies also have showed that the hepatotoxic effect of tacrine is associated with oxidative stress, as demonstrated by increased reactive oxygen species (ROS) production and decreased intracellular glutathione (GSH).6-8) However, mechanism responsible for tacrine-induced hepatotoxicity has not yet been elucidated. Nevertheless many studies have shown that anthraquinones, chromone glycosides, phenolic amide, and an herbal medicine protect hepatocytes from the toxic effects of tacrine. [9][10][11][12] Oxidative stress is state in which the balance between ROS production and antioxidants is shifted in favor of ROS, and is associated with severity of liver damage.13) ROS normally work ...

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Liquiritigenin, an aglycone of liquiritin in Glycyrrhizae radix, prevents acute liver injuries in rats induced by acetaminophen with or without buthionine sulfoximine

Cited by 108 publications

References 24 publications

Liquiritigenin inhibits Aβ25–35-induced neurotoxicity and secretion of Aβ1–40 in rat hippocampal neurons

Liquiritigenin inhibits Aβ25–35-induced neurotoxicity and secretion of Aβ1–40 in rat hippocampal neurons

Production of Liquiritigenin with Cell-based Biotransformation and Its Anti-Aging Activity

Tacrine, an Oral Acetylcholinesterase Inhibitor, Induced Hepatic Oxidative Damage, Which Was Blocked by Liquiritigenin through GSK3-beta Inhibition

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