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  • beta-香树精

    beta-Amyrin

    beta-香树精
    产品编号 CFN98935
    CAS编号 559-70-6
    分子式 = 分子量 C30H50O = 426.7
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Triterpenoids
    植物来源 The stem barks of Alstonia boonei
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    beta-香树精 CFN98935 559-70-6 1mg QQ客服:1413575084
    beta-香树精 CFN98935 559-70-6 5mg QQ客服:1413575084
    beta-香树精 CFN98935 559-70-6 10mg QQ客服:1413575084
    beta-香树精 CFN98935 559-70-6 20mg QQ客服:1413575084
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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
  • Seoul National University (Korea)
  • Macau University of Science and Technology (China)
  • Universite Libre de Bruxelles (Belgium)
  • Kamphaengphet Rajabhat University (Thailand)
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  • Massachusetts General Hospital (USA)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • J.Acta Agriculturae Scandinavica2017, 571-575
  • J Ethnopharmacol.2016, 192:370-381
  • GENENCELL2023, 25:4356740
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  • Advances in Traditional Medicine2020, 10.1007
  • Am J Chin Med.2016, 44(8):1719-1735
  • J Pharm Biomed Anal.2016, 129:50-59
  • Mol Pharmacol.2021, 99(2):163-174.
  • J Nat Med.2018, 72(3):734-744
  • Journal of Functional Foods2022, 91:105019.
  • Russian J Bioorganic Chemistry 2021, 47:1411-1417.
  • Nutrients.2020, 12(11):3448.
  • Mutlu Yanic S, Ates EG. JOTCSA.2023, 10(4);893-902.
  • Hum Exp Toxicol.2023, 42:9603271231171642.
  • J Nat Med.2017, 71(2):457-462
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  • ...
  • 生物活性
    Description: beta-Amyrin has antiviral, hepatoprotective, antinociceptive, anti-inflammatory, it retard acute inflammation in rat model of periodontitis. Beta-Amyrin can enhance the total sleeping behavior in pentobarbital-induced sleeping model via the activation of GABAergic neurotransmitter system through GABA content in the brain.alpha- and beta-Amyrin mixture has gastro-protective activity, the mechanism involves at least in part the activation of capsaicin-sensitive primary afferent neurons; it also has sedative and anxiolytic effects, the mechanism may involve an action on benzodiazepine-type receptors, and also an antidepressant effect where noradrenergic mechanisms will probably play a role.
    Targets: GABA Receptor | P450 (e.g. CYP17) | cAMP | PKC | PKA | PGE | TNF-α | Antifection
    In vitro:
    J Pharm Sci. 1974 Mar;63(3):471-3.
    Antiviral activity of triterpenoid saponins containing acylated beta-amyrin aglycones.[Pubmed: 4820390]
    Antiviral activity of triterpenoid saponins containing acylated beta-amyrin aglycones.
    In vivo:
    Pharm Biol. 2014 Nov;52(11):1478-86.
    beta-Amyrin and alpha-amyrin acetate isolated from the stem bark of Alstonia boonei display profound anti-inflammatory activity.[Pubmed: 25026352]
    Alstonia boonei De Wild (Apocyanaceae) is used in ethnomedicine for the management of malaria, ulcer, rhematic pain, toothache, and inflammatory disorders.To investigate the anti-inflammatory potential of beta-Amyrin and α-amyrin acetate isolated from the stem bark of Alstonia boonei using animal models.
    METHODS AND RESULTS:
    Chromatographic purification of the crude methanol extract led to the isolation and structure elucidation of beta-Amyrin and α-amyrin acetate. Their anti-inflammatory activities were evaluated in rodents using egg albumen-induced paw edema and xylene-induced ear edema models. The gastric ulcerogenic, in vivo leucocyte migration, and RBC membrane stabilization tests were also investigated. α-Amyrin acetate at 100 mg/kg showed significant (p < 0.05) inhibition of egg albumen-induced paw edema with % inhibition of 40 at the 5th hour. Oral administration up to 100 mg/kg did not produce significant (p > 0.01) irritation of the gastric mucosa while significant (p < 0.01) ulceration was recorded for indomethacin at 40 mg/kg compared with the negative control. At 100 μg/mL, both beta-Amyrin and α-amyrin acetate inhibited heat-induced hemolysis to as much 47.2 and 61.5%, respectively, while diclofenac sodium (100 μg/mL) evoked only 40.5% inhibition. Both compounds at 100 µg/ear produced significant (p < 0.01) inhibition of ear edema in mice by 39.4 and 55.5%, respectively. Also at 100 mg/kg (p.o.) α-amyrin acetate evoked 60.3% reduction in total leucocyte count and significant (p < 0.05) suppression (47.9%) of neutrophil infiltration.
    CONCLUSIONS:
    This study generally provided evidence of profound anti-inflammatory activity of β-amyrin and α-amyrin acetate isolated from the Alstonia boonei stem bark.
    J Pharmacol Exp Ther. 2005 Apr;313(1):310-8.
    Antinociceptive properties of mixture of alpha-amyrin and beta-amyrin triterpenes: evidence for participation of protein kinase C and protein kinase A pathways.[Pubmed: 15626726 ]

    METHODS AND RESULTS:
    The mixture of the two pentacyclic triterpenes alpha-amyrin and beta-amyrin, isolated from the resin of Protium kleinii and given by intraperitoneal (i.p.) or oral (p.o.) routes, caused dose-related and significant antinociception against the visceral pain in mice produced by i.p. injection of acetic acid. Moreover, i.p., p.o., intracerebroventricular (i.c.v.), or intrathecal (i.t.) administration of alpha,beta-amyrin inhibited both neurogenic and inflammatory phases of the overt nociception caused by intraplantar (i.pl.) injection of formalin. Likewise, alpha,beta-amyrin given by i.p., p.o., i.t., or i.c.v. routes inhibits the neurogenic nociception induced by capsaicin. Moreover, i.p. treatment with alpha,beta-amyrin was able to reduce the nociception produced by 8-bromo-cAMP (8-Br-cAMP) and by 12-O-tetradecanoylphorbol-13-acetate (TPA) or the hyperalgesia caused by glutamate. On the other hand, in contrast to morphine, alpha,beta-amyrin failed to cause analgesia in thermal models of pain. The antinociception caused by the mixture of compounds seems to involve mechanisms independent of opioid, alpha-adrenergic, serotoninergic, and nitrergic system mediation, since it was not affected by naloxone, prazosin, yohimbine, DL-p-chlorophenylalanine methyl ester, or L-arginine. Interestingly, the i.p. administration of alpha,beta-amyrin reduced the mechanical hyperalgesia produced by i.pl. injection of carrageenan, capsaicin, bradykinin, substance P, prostaglandin E2, 8-Br-cAMP, and TPA in rats. However, the mixture of compounds failed to alter the binding sites of [3H]bradykinin, [3H]resiniferatoxin, or [3H]glutamate in vitro.
    CONCLUSIONS:
    It is concluded that the mixture of triterpene alpha-amyrin and beta-amyrin produced consistent peripheral, spinal, and supraspinal antinociception in rodents, especially when assessed in inflammatory models of pain. The mechanisms involved in their action are not completely understood but seem to involve the inhibition of protein kinase A- and protein kinase C-sensitive pathways.
    Inflammopharmacology. 2008 Feb;16(1):48-52.
    Anti-inflammatory effect of alpha, beta-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis.[Pubmed: 18046512 ]
    This study was aimed to evaluate the anti-inflammatory potential of triterpene alpha, beta-Amyrin in rats on acute phase periodontitis.
    METHODS AND RESULTS:
    Periodontitis was induced by ligature placement around the maxillary right second molar tooth. Rats (n = 8/group) were pretreated with alpha, beta-Amyrin (5 and 10 mg/kg, p. o.), two hours before the induction of periodontal inflammation. Sham-operated and positive controls (lumiracoxib and dexamethasone) were included. Six hours later, plasma levels of TNF-alpha were analysed. Rats were sacrificed at 24 h, and the gingival tissue analysed for myeloperoxidase (MPO) and thiobarbituric acid-reactive substances (TBARS), as measures of neutrophil influx and lipid-peroxidation, respectively alpha, beta-Amyrin as well as dexamethasone significantly inhibited the periodontitis-associated increases of TNF-alpha, and the gingival MPO and TBARS. alpha, beta-Amyrin effect was more prominent at 5 mg/kg. Lumiracoxib manifested varied influence on the studied parameters.
    CONCLUSIONS:
    These results provide evidence to show that alpha, beta-Amyrin retards acute inflammation in rat model of periodontitis and warrant further study on its efficacy to prevent chronic periodontitis-associated bone loss.
    Pharmacol Biochem Behav. 2006 Dec;85(4):827-34.
    A possible mechanism for anxiolytic and antidepressant effects of alpha- and beta-amyrin from Protium heptaphyllum (Aubl.) March.[Pubmed: 17207523 ]
    In the present study, we examined the anxiolytic and antidepressant effects of the mixture of alpha- and beta-Amyrin (AMY), pentacyclic triterpenes isolated from the stem bark resin of Protium heptaphyllum.
    METHODS AND RESULTS:
    These effects of AMY were demonstrated by the open-field, elevated-plus-maze, rota rod, forced swimming, and pentobarbital-induced sleeping time tests, in mice. In the open-field test, AMY at the doses of 10, 25 and 50 mg/kg, after intraperitoneal or oral administrations, significantly decreased the number of crossings, grooming, and rearing. All these effects were reversed by the pre-treatment with flumazenil (2.5 mg/kg, i.p.), similarly to those observed with diazepam used as a positive standard. In the elevated-plus-maze test, AMY increased the time of permanence and the number of entrances in the open arms. On the contrary, the time of permanence and the number of entrances in the closed arms were decreased. All these effects were also completely reversed by flumazenil, an antagonist of benzodiazepine receptors. In the pentobarbital-induced sleeping time test, AMY at the same doses significantly increased the animals sleeping time duration. In the rota rod test, AMY did not alter motor coordination and, thus, was devoid of effects, as related to controls. Since AMY, at the doses of 10 and 25 mg/kg, showed a sedative effect in the open field test, lower doses (2.5 and 5.0 mg/kg) were used in the forced swimming test, producing a decrease in the immobility time, similarly to that of imipramine, the positive control. The effect of AMI was greater when it was administered 15 min after imipramine (10 mg/kg). However, the antidepressant AMY effects were not altered by the previous administration of paroxetine, a selective blocker of serotonin uptake. In addition, AMY effects in the forced swimming test were totally blocked by reserpine pretreatment, a drug known to induce depletion of biogenic amines.
    CONCLUSIONS:
    In conclusion, the present work evidenced sedative and anxiolytic effects of AMY that might involve an action on benzodiazepine-type receptors, and also an antidepressant effect where noradrenergic mechanisms will probably play a role.
    Biomol Ther (Seoul) . 2020 Jan 1;28(1):74-82.
    β-Amyrin Ameliorates Alzheimer's Disease-Like Aberrant Synaptic Plasticity in the Mouse Hippocampus[Pubmed: 31357749]
    Alzheimer's disease (AD) is a progressive and most frequently diagnosed neurodegenerative disorder. However, there is still no drug preventing the progress of this disorder. β-Amyrin, an ingredient of the surface wax of tomato fruit and dandelion coffee, is previously reported to ameliorate memory impairment induced by cholinergic dysfunction. Therefore, we tested whether β-amyrin can prevent AD-like pathology. β-Amyrin blocked amyloid β (Aβ)-induced long-term potentiation (LTP) impairment in the hippocampal slices. Moreover, β-amyrin improved Aβ-induced suppression of phosphatidylinositol-3-kinase (PI3K)/Akt signaling. LY294002, a PI3K inhibitor, blocked the effect of β-amyrin on Aβ-induced LTP impairment. In in vivo experiments, we observed that β-amyrin ameliorated object recognition memory deficit in Aβ-injected AD mice model. Moreover, neurogenesis impairments induced by Aβ was improved by β-amyrin treatment. Taken together, β-amyrin might be a good candidate of treatment or supplement for AD patients.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.3436 mL 11.7178 mL 23.4357 mL 46.8713 mL 58.5892 mL
    5 mM 0.4687 mL 2.3436 mL 4.6871 mL 9.3743 mL 11.7178 mL
    10 mM 0.2344 mL 1.1718 mL 2.3436 mL 4.6871 mL 5.8589 mL
    50 mM 0.0469 mL 0.2344 mL 0.4687 mL 0.9374 mL 1.1718 mL
    100 mM 0.0234 mL 0.1172 mL 0.2344 mL 0.4687 mL 0.5859 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
    13(18)-齐墩果烯-3-酮,Α-香树脂酮; 13(18)-Oleanen-3-one CFN98023 20248-08-2 C30H48O = 424.7 5mg QQ客服:1413575084
    台湾牛奶菜双氧甾甙 B; Marsformoxide B CFN96397 2111-46-8 C32H50O3 = 482.8 5mg QQ客服:215959384
    (3beta,11alpha,12alpha,13alpha)-11,12-环氧-13-甲基-27-去甲齐墩果-14-烯-3-醇十六烷酸酯 ; 11alpha,12alpha-Oxidotaraxerol palmitate CFN96827 495389-95-2 C46H78O3 = 679.11 5mg QQ客服:1413575084
    大豆甾醇A; Soyasapogenol A CFN93150 508-01-0 C30H50O4 = 474.7 5mg QQ客服:2159513211
    日耳曼醇; Germanicol CFN89221 465-02-1 C30H50O = 426.72 5mg QQ客服:1457312923
    Germanicol acetate ; Germanicol acetate CFN96961 10483-91-7 C32H52O2 = 468.76 5mg QQ客服:1413575084
    beta-香树脂醇乙酸酯; beta-Amyrin acetate CFN99679 1616-93-9 C32H52O2 = 468.8 5mg QQ客服:2159513211
    beta-软脂酸香树精酯; beta-Amyrin palmitate CFN97009 5973-06-8 C46H80O2 = 665.1 5mg QQ客服:3257982914
    beta-白檀酮; beta-Amyrone CFN97099 638-97-1 C30H48O = 424.7 5mg QQ客服:2159513211
    9(11),12-齐墩果二烯-3beta-醇; 9(11),12-Oleanadien-3-ol CFN97528 94530-87-7 C30H48O = 424.7 5mg QQ客服:2159513211

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