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  • 甘草酸

    Glycyrrhizic acid

    甘草酸
    产品编号 CFN99151
    CAS编号 1405-86-3
    分子式 = 分子量 C42H62O16 = 822.92
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Triterpenoids
    植物来源 The roots of Glycyrrhiza glabra L.
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • University of South Australia (Australia)
  • St. Jude Children Research Hospital (USA)
  • National Research Council of Canada (Canada)
  • Kyoto University (Japan)
  • Amity University (India)
  • Shanghai Institute of Organic Chemistry (China)
  • Centrum Menselijke Erfelijkheid (Belgium)
  • Max-Planck-Insitut (Germany)
  • Florida International University (USA)
  • Chinese University of Hong Kong (China)
  • Guangzhou Institutes of Biomedicine and Health (China)
  • The Ohio State University (USA)
  • Universitas islam negeri Jakarta (Indonesia)
  • Universit?t Basel (Switzerland)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Srinagarind Medical Journal2019, 34(1)
  • Sci Rep.2017, 7:46299
  • Curr Issues Mol Biol.2023, 45(3):2136-2156.
  • Biosci Biotechnol Biochem.2020, 84(3):621-632
  • Phytomedicine.2022, 99:153997.
  • J Inflamm Res.2022, 15:5347-5359.
  • Nutrients.2019, 12(1):E40
  • Evid Based Complement Alternat Med.2016, 2016:1739760
  • Eur Rev Med Pharmacol Sci.2020, 24(9):5127-5139.
  • Chemistry of Vegetable Raw Materials2019, 3:119-127
  • Planta Med.2018, 84(15):1101-1109
  • Nutrients.2019, 11(6):E1380
  • Korean J. Crop Sci.2018, 63(2):131-139
  • Molecules.2020, 25(23):5556.
  • Front Microbiol.2020, 11:583594.
  • Pathogens.2018, 7(3):E62
  • Nutrients.2019, 11(4):E936
  • Rev. Chim.2020, 71(3),558-564
  • J Cell Mol Med.2023, 27(10):1423-1435.
  • China Pharmacy2015, 26(27)
  • Front Pharmacol.2022, 13:806869.
  • Appl. Sci. 2021, 11(22),10569
  • Int J Mol Sci.2020, 21(9):3392.
  • ...
  • 生物活性
    Description: Glycyrrhizic acid has anti-tumor, antiviral ,antiallergic, anti-inflammatory, immunoregulatory,anti-diabetic activities. It is a direct HMGB1(high mobility group box 1) inhibitor that inhibits HMGB1-dependent inflammatory molecule expression and oxidative stress; modulates P38 and P-JNK but not p-ERK signalling; Also inhibits 11 beta-hydroxysteroid dehydrogenase and monoamine oxidase (MAO).
    Targets: NO | PGE | ROS | NOS | COX | TNF-α | NF-kB | PI3K | IL Receptor | Antifection
    In vitro:
    J Agric Food Chem. 2011 Jul 27;59(14):7726-33.
    Glycyrrhizic acid and 18β-glycyrrhetinic acid modulate lipopolysaccharide-induced inflammatory response by suppression of NF-κB through PI3K p110δ and p110γ inhibitions.[Pubmed: 21644799]
    The roots and rhizomes of licorice ( Glycyrrhia ) species have been used extensively as natural sweeteners and herbal medicines.
    METHODS AND RESULTS:
    The aim of this work was to determine the in vitro anti-inflammatory effects of glycyrrhizic acid (GA) and 18β-glycyrrhetinic acid (18βGA) from licorice in a lipopolysaccharide (LPS)-stimulated macrophage model. The results showed that treatment with 25-75 μM GA or 18βGA did not reduce RAW 264.7 cell viability but did significantly inhibit the production of LPS-induced nitric oxide (NO), prostaglandin E(2) (PGE(2)), and intracellular reactive oxygen species (ROS). Western blotting and reverse transcriptase polymerase chain reaction (RT-PCR) analyses revealed that GA and 18βGA significantly reduced the protein and mRNA levels of iNOS and COX-2 in LPS-induced macrophages. Both GA and 18βGA inhibited the activation of NF-κB and the activities of phosphoinositide-3-kinase (PI3K) p110δ and p110γ isoforms and then reduced the production of LPS-induced tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β in a dose-dependent manner. In conclusion, these results indicate that GA and 18βGA may provide an anti-inflammatory effect by attenuating the generation of excessive NO, PGE(2), and ROS and by suppressing the expression of pro-inflammatory genes through the inhibition of NF-κB and PI3K activity.
    CONCLUSIONS:
    Thus, the results suggest that GA and 18βGA might serve as potential agents for the treatment of inflammatory-mediated diseases.
    J Ethnopharmacol. 2013 May 2;147(1):114-21.
    Glycyrrhizic acid as the antiviral component of Glycyrrhiza uralensis Fisch. against coxsackievirus A16 and enterovirus 71 of hand foot and mouth disease.[Pubmed: 23454684 ]
    The radices of Glycyrrhiza uralensis Fisch. and herbal preparations containing Glycyrrhiza spp. have been used for thousands of years as an herbal medicine for the treatment of viral induced cough, viral hepatitis, and viral skin diseases like ulcers in China. Glycyrrhizic acid (GA) is considered the principal component in Glycyrrhiza spp. with a wide spectrum of antiviral activity. The present study attempt to validate the medicinal use of Glycyrrhiza uralensis for hand, foot and mouth disease (HFMD) and further to verify whether GA is an active antiviral component in the water extract of Glycyrrhiza uralensis.
    METHODS AND RESULTS:
    Radices of Glycyrrhiza uralensis Fisch. were extracted with hot water. The chemical contents of the extract were profiled with HPLC analysis. The antiviral activity of the extract and the major components was evaluated against infection of enterovirus 71 (EV71) and coxsackievirus A16 (CVA16) on Vero cells. The cytopathic effect caused by the infection was measured with MTT assay. Infectious virion production was determined using secondary infection assays and viral protein expression by immunoblotting analysis. The extract at 1000 μg/ml suppressed EV71 replication by 1.0 log and CVA16 by 1.5 logs. The antiviral activity was associated with the content of GA in the extract since selective depletion of GA from the extract by acid precipitation resulted in loss of antiviral activity. In contrast, the acid precipitant retained antiviral activity. The precipitant at a concentration of 200 μg/ml inhibited EV71 and CVA16 replication by 1.7 and 2.2 logs, respectively. Furthermore, GA dose-dependently blocked viral replication of EV71 and CVA16. At 3 mM, GA reduced infectious CVA16 and EV71 production by 3.5 and 2.2 logs, respectively. At 5mM, CVA16 production was reduced by 6.0 logs and EV71 by 4.0 logs. Both EV71 and CVA16 are members of Enterovirus genus, time-of-drug addition studies however showed that GA directly inactivated CVA16, while GA anti-EV71 effect was associated with an event(s) post virus cell entry.
    CONCLUSIONS:
    This study validated the medicinal usefulness of radices Glycyrrhiza uralensis against the etiological agents of HFMD. In addition to the identification of GA as the antiviral component of Glycyrrhiza uralensis against EV71 and CVA16 infection, this study also reveals that GA inhibits EV71 and CVA16 with distinct mechanisms.
    Biomed Pharmacother . 2017 Nov;95:670-678.
    Glycyrrhizic acid: A promising carrier material for anticancer therapy[Pubmed: 28886526]
    Drug delivery systems have become an integral part of anticancer drugs today. Design of novel drug carriers may lead to significant enhancement in antineoplastic therapy. Glycyrrhizic acid (GL), which is the most important active ingredient extracted from the licorice root shows great potential as a carrier material in this field. Recent studies have indicated that the combination of GL and first-line drugs had better therapeutic effects on cancers. GL showed a series of anti-cancer-related pharmacological activities, such as broad-spectrum anti-cancer ability, resistance to the tissue toxicity caused by chemotherapy and radiation, drug absorption enhancing effects and anti-multidrug resistance (MDR) mechanisms, as a carrier material in drug delivery systems. This review introduced the current research progress on pharmacological mechanisms of GL and development of GL-based drug carriers in anti-cancer field to provide basis for the application prospects of GL. The design of novel GL-based drug delivery systems will bring new opportunities and challenges to anti-cancer therapy.
    Biomed Pharmacother . 2017 Nov;95:599-604.
    Glycyrrhizic acid increases glucagon like peptide-1 secretion via TGR5 activation in type 1-like diabetic rats[Pubmed: 28881290]
    Glycyrrhizic acid (GA) is belonged to triterpenoid saponin that is contained in the root of licorice and is known to affect metabolic regulation. Recently, glucagon like peptide-1 (GLP-1) has widely been applied in diabetes therapeutics. However, the role of GLP-1 in GA-induced anti-diabetic effects is still unknown. Therefore, we are interested in understanding the association of GLP-1 with GA-induced effects. In type 1-like diabetic rats induced by streptozotocin (STZ-treated rats), GA increased the level of plasma GLP-1, which was blocked by triamterene at a dose sufficient to inhibit Takeda G-protein-coupled receptor 5 (TGR5). The direct effect of GA on TGR5 has been identified using the cultured Chinese hamster ovary cells (CHO-K1 cells) transfected TGR5 gene. Moreover, in intestinal NCI-H716 cells that secreted GLP-1, GA promoted GLP-1 secretion with a marked elevation of calcium levels. However, both effects of GA were reduced by ablation of TGR5 with siRNA in NCI-H716 cells. Therefore, we demonstrated that GA can enhance GLP-1 secretion through TGR5 activation.
    In vivo:
    Am J Nephrol. 2014;40(1):84-95.
    Glycyrrhizic acid ameliorates HMGB1-mediated cell death and inflammation after renal ischemia reperfusion injury.[Pubmed: 25059568]
    Renal ischemia reperfusion injury (IRI) leads to acute kidney injury (AKI) and the death of tubular epithelial cells (TEC). The release of high-mobility group box-1 (HMGB1) and other damage-associated molecular pattern moieties from dying cells may promote organ dysfunction and inflammation by effects on TEC. Glycyrrhizic acid (GZA) is a functional inhibitor of HMGB1, but its ability to attenuate the HMGB1-mediated injury of TEC has not been tested.
    METHODS AND RESULTS:
    In vitro, hypoxia and cytokine treatment killed TEC and resulted in the progressive release of HMGB1 into the supernatant. GZA reduced the hypoxia-induced TEC death as measured by annexin-V and propidium iodide. Hypoxia increased the expression of MCP-1 and CXCL1 in TEC, which was reduced by GZA in a dose-dependent manner. Similarly, the HMGB1 activation of effector NK cells was inhibited by GZA. To test the effect of HMGB1 neutralization by GZA in vivo, mice were subjected to renal IRI. HMGB1 protein expression increased progressively in kidneys from 4 to 24 h after ischemia and was detected in tubular cells by 4 h using immunohistochemistry. GZA preserved renal function after IRI and reduced tubular necrosis and neutrophil infiltration by histological analyses and ethidium homodimer staining.
    CONCLUSIONS:
    Importantly, these data demonstrate for the first time that AKI following hypoxia and renal IRI may be promoted by HMGB1 release, which can reduce the survival of TEC and augment inflammation. Inhibition of the interaction of HMGB1 with TEC through GZA may represent a therapeutic strategy for the attenuation of renal injury following IRI and transplantation.
    Biomed Res Int. 2014;2014:872139.
    Glycyrrhizic acid in the treatment of liver diseases: literature review.[Pubmed: 24963489]
    Glycyrrhizic acid (GA) is a triterpene glycoside found in the roots of licorice plants (Glycyrrhiza glabra). GA is the most important active ingredient in the licorice root, and possesses a wide range of pharmacological and biological activities. GA coupled with glycyrrhetinic acid and 18-beta-glycyrrhetic acid was developed in China or Japan as an anti-inflammatory, antiviral, and antiallergic drug for liver disease. This review summarizes the current biological activities of GA and its medical applications in liver diseases. The pharmacological actions of GA include inhibition of hepatic apoptosis and necrosis; anti-inflammatory and immune regulatory actions; antiviral effects; and antitumor effects.
    CONCLUSIONS:
    This paper will be a useful reference for physicians and biologists researching GA and will open the door to novel agents in drug discovery and development from Chinese herbs. With additional research, GA may be more widely used in the treatment of liver diseases or other conditions.
    Thyroid . 2017 May;27(5):722-731.
    Glycyrrhizin, a Direct HMGB1 Antagonist, Ameliorates Inflammatory Infiltration in a Model of Autoimmune Thyroiditis via Inhibition of TLR2-HMGB1 Signaling[Pubmed: 28363255]
    Background: High mobility group box-1 (HMGB1), a non-histone protein, plays an important role in autoimmune diseases. However, the significance of HMGB1 in the pathogenesis of autoimmune thyroiditis has not been reported. The purpose of this study was to explore whether HMGB1 participates in the pathogenesis of autoimmune thyroiditis, and whether glycyrrhizin (GL), a direct inhibitor of HMGB1, attenuates the severity of thyroid inflammatory infiltration in a murine model of autoimmune thyroiditis. Methods: A total of 80 male NOD.H-2h4 mice were randomly divided into a control or iodine supplement (NaI) group at four weeks of age, and the control group was fed with regular water, whereas the NaI group was supplied with 0.005% sodium iodine water. Another 24 male NOD.H-2h4 mice were also randomized into three groups (eight mice per group) as follows: control, NaI, and GL treatment after iodine supplementation (NaI + GL). The NOD.H-2h4 mice were fed with 0.005% sodium iodide water for eight weeks to enhance autoimmune thyroiditis. After iodine treatment, the mice received intraperitoneal injections of GL for four weeks. The severity of lymphocytic infiltration in the thyroid gland was measured by histopathological studies. The serum levels of HMGB1, tumor necrosis factor alpha, interleukin (IL)-6, IL-1β, and thyroglobulin antibody titers were measured using an enzyme-linked immunosorbent assay. HMGB1 expression was measured by immunohistochemical staining and real-time polymerase chain reaction. TLR2, HMGB1, MyD88, and nuclear transcription factor κB were measured by Western blot. Results: The mRNA expression of HMGB1 was significantly higher at 8 and 16 weeks in the NaI group than it was in the control group. Serum levels of thyroglobulin antibodies, HMGB1, tumor necrosis factor alpha, IL-6, and IL-1β were significantly increased in the NaI group, but they were dramatically attenuated with GL injection. The prevalence of thyroiditis and the infiltration of lymphocytes were significantly decreased in the NaI + GL group. GL administration also significantly reduced the protein expression of TLR2, MyD88, HMGB1 and nuclear transcription factor κB in the thyroid gland and attenuated the severity of thyroiditis. Conclusion: HMGB1 may play a crucial role in autoimmune thyroiditis by causing inflammatory infiltration, thus increasing the severity of autoimmune thyroiditis. GL effectively attenuated thyroiditis in the iodine-induced NOD.H-2h4 mice via a molecular mechanism related to the inhibition of TLR2-HMGB1 signaling.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.2152 mL 6.0759 mL 12.1518 mL 24.3037 mL 30.3796 mL
    5 mM 0.243 mL 1.2152 mL 2.4304 mL 4.8607 mL 6.0759 mL
    10 mM 0.1215 mL 0.6076 mL 1.2152 mL 2.4304 mL 3.038 mL
    50 mM 0.0243 mL 0.1215 mL 0.243 mL 0.4861 mL 0.6076 mL
    100 mM 0.0122 mL 0.0608 mL 0.1215 mL 0.243 mL 0.3038 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    商陆皂苷乙; Esculentoside B CFN98163 60820-94-2 C36H56O11 = 664.82 5mg QQ客服:2159513211
    商陆皂苷丁; Esculentoside D CFN98165 89808-50-4 C37H58O12 = 694.85 5mg QQ客服:3257982914
    商陆皂苷丙; Esculentoside C CFN98164 65931-92-2 C42H66O15 = 810.97 5mg QQ客服:215959384
    商陆皂苷甲; Esculentoside A CFN98162 65497-07-6 C42H66O16 = 826.96 20mg QQ客服:215959384
    商陆皂苷辛; Esculentoside H CFN90657 66656-92-6 C48H76O21 = 989.1 20mg QQ客服:1413575084
    商陆皂苷T; Esculentoside T CFN90658 N/A C42H64O16 = 824.4 20mg QQ客服:3257982914
    百两金素A; Ardisiacrispin A CFN90177 23643-61-0 C52H84O22 = 1061.21 5mg QQ客服:1413575084
    百两金皂苷B; Ardisiacrispin B CFN91120 112766-96-8 C53H86O22 = 1075.3 5mg QQ客服:215959384
    朱砂根皂苷A; Ardisicrenoside A CFN91122 160824-52-2 C53H88O22 = 1077.3 5mg QQ客服:3257982914
    单葡萄糖醛酸甘草次酸; Glycyrrhetic acid 3-O-mono-beta-D-glucuronide CFN90683 34096-83-8 C36H54O10 = 646.8 5mg QQ客服:2159513211

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