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  • 茯苓酸; 茯灵酸

    Pachymic acid

    茯苓酸; 茯灵酸
    产品编号 CFN99590
    CAS编号 29070-92-6
    分子式 = 分子量 C33H52O5 = 528.76
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Triterpenoids
    植物来源 The roots of Wolfiporia cocos (Schw.) Ryv.
    产品名称 产品编号 CAS编号 包装 QQ客服
    茯苓酸; 茯灵酸 CFN99590 29070-92-6 10mg QQ客服:2056216494
    茯苓酸; 茯灵酸 CFN99590 29070-92-6 20mg QQ客服:2056216494
    茯苓酸; 茯灵酸 CFN99590 29070-92-6 50mg QQ客服:2056216494
    茯苓酸; 茯灵酸 CFN99590 29070-92-6 100mg QQ客服:2056216494
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  • ...
  • 生物活性
    Description: Pachymic acid has sedative-hypnotic, cardioprotective,antioxidant, and anti-inflammatory activities, it has hypoglycemic activity ,can stimulate glucose uptake, GLUT4 gene expression and translocation, and promoting triglyceride accumulation in adipocytes. Pachymic acid may inhibit proliferation and invasion of ovarian carcinoma cell through decreasing β-catenin and COX-2 expression and increasing E-cadherin exprssion. Pachymic acid is suggested to prevent the complications of oral diseases such as inflammation and alveolar destruction of the oral cavity.
    Targets: Nrf2 | TNF-α | IL Receptor | NF-kB | HO-1 | COX | Caspase | ERK | p38MAPK | GLUT | PI3K | AMPK | Akt | GABA Receptor
    In vitro:
    J Endod. 2013 Apr;39(4):461-6.
    The antioxidant property of pachymic acid improves bone disturbance against AH plus-induced inflammation in MC-3T3 E1 cells.[Pubmed: 23522537]
    The cytotoxicity of resin-based sealer is influential on the inflammatory reaction and cell survival for oral periapical cells. In this study, pachymic acid as an antioxidant was investigated for the improvement of bone disturbance against AH Plus (Dentsply DeTrey GmbH, Konstanz, Germany)-induced inflammation in MC-3T3 E1 cells.
    AH Plus was prepared according to the manufacturer's instructions. Using mouse osteoblast cells (MC-3T3 E1), a specimen of AH Plus was eluted with the culture medium for 1 day and was diluted by 30%. The cellular cytotoxicity and reactive oxygen species formation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 2',7'-dichlorodihydrofluorescein diacetate with fluorescence-activated cell sorting. The secretion of proinflammatory cytokines was determined by an enzyme-linked immunosorbent assay, and the expression of inflammatory and osteogenic molecules was determined by immunoblotting. Cells with AH Plus elutes showed a decrease of cell viability and ALP activity. However, pachymic acid and N-acetyl-L-cysteine (control antioxidant) restored cell viability and ALP activity damaged by AH plus. The secretion of nitric oxide, tumor necrosis factor α, and interleukin-1β were increased in AH Plus-stimulated MC-3T3 E1 cells, but pachymic acid suppressed its production. Furthermore, pachymic acid reduced the receptor activator of nuclear factor-κB ligand, cyclooxygenase-2, matrix metalloproteinase-2 and -9, increased bone morphogenetic protein-2 and -7, and runt-related transcription factor 2 despite AH Plus stimuli. In addition, pachymic acid affected the removal effect of reactive oxygen species formation as did N-acetyl-L-cysteine. More importantly, pachymic acid inhibited nuclear factor-κB translocation.
    The property of pachymic acid can mitigate the unfavorable conditions induced by AH Plus stimuli. Therefore, the use of pachymic acid is suggested to prevent the complications of oral diseases such as inflammation and alveolar destruction of the oral cavity.
    Eur J Pharmacol. 2010 Dec 1;648(1-3):39-49.
    Pachymic acid stimulates glucose uptake through enhanced GLUT4 expression and translocation.[Pubmed: 20816811 ]
    In an effort to investigate the effect and mechanism of Poria cocos on glucose uptake, six lanostane-type triterpenoids were isolated and analyzed.
    Among them, pachymic acid displayed the most significant stimulating activity on glucose uptake in 3T3-L1 adipocytes. The effect of pachymic acid on the expression profile of glucose transporters in differentiated 3T3-L1 adipocytes was also analyzed. Our results demonstrated that pachymic acid induced an increase in GLUT4, but not GLUT1, expression at both the mRNA and protein levels. The role of GLUT4 was further confirmed using the lentiviral vector-derived GLUT4 short hairpin RNA (shRNA). The stimulating activity of pachymic acid on glucose uptake was abolished when the endogenous GLUT4 expression was suppressed in 3T3-L1 adipocytes. In addition to increased GLUT4 expression, pachymic acid stimulated GLUT4 redistribution from intracellular vesicles to the plasma membrane in adipocytes. Exposure of the differentiated adipocytes to pachymic acid increased the phosphorylation of insulin receptor substrate (IRS)-1, AKT and AMP-activated kinase (AMPK). The involvement of PI3K and AMPK in the action of pachymic acid was further confirmed as PI3K and AMPK inhibitors completely blocked the pachymic acid-mediated activities in adipocytes. In addition, pachymic acid was shown to induce triglyceride accumulation and inhibit lipolysis in differentiated adipocytes.
    Taken together, we demonstrated the insulin-like activities of this compound in stimulating glucose uptake, GLUT4 gene expression and translocation, and promoting triglyceride accumulation in adipocytes. Our study provides important insights into the underlying mechanism of hypoglycemic activity of P. cocos.
    2015 Oct 15;8(10):17781-8.
    Pachymic acid inhibits tumorigenesis in gallbladder carcinoma cells[Pubmed: 26770369]
    Abstract Background: Gallbladder cancer, with high aggressivity and extremely poor prognosis, is the most common malignancy of the bile duct. Thus, seeking targets gallbladder tumor cells is an attractive goal towards improving clinical treatment. Material and methods: In this study, we investigated the effects of pachymic acid (PA) on the tumorigenesis of human gallbladder cancer cells. Results: We found that PA significantly reduced cell growth in a dose- and time-dependent fashion. Meanwhile, cell cycle arrest at G0 phase was induced by PA. PA also significantly inhibited cancer cell migration, invasion in a dose-dependent manner. Interestingly, we demonstrated that cancer cell adhesion ability was suppressed dose-dependently, which may contribute to the inhibition of cell invasion. Finally, we showed that PA inhibited AKT and ERK signaling pathways. And oncoproteins, such as PCNA, ICAM-1 and RhoA which are involved intumorigenesis, were also downregulated by PA. Conclusion: Our study reveals that PA is able to inhibit gallbladder cancer tumorigenesis involving affection of AKT and ERK signaling pathways. Together, these results encourage further studies of PA as a promising candidate for gallbladder cancer therapy. Keywords: Pachymic acid; adhesion; gallbladder cancer; growth; invasion; migration.
    In vivo:
    Biomol Ther (Seoul). 2014 Jul; 22(4): 314–20.
    Pachymic Acid Enhances Pentobarbital-Induced Sleeping Behaviors via GABAA-ergic Systems in Mice[Pubmed: 25143810]
    This study was investigated to know whether pachymic acid (PA), one of the predominant triterpenoids in Poria cocos (Hoelen) has the sedative-hypnotic effects, and underlying mechanisms are mediated via γ-aminobutyric acid (GABA)-ergic systems.
    Oral administration of PA markedly suppressed locomotion activity in mice. This compound also prolonged sleeping time, and reduced sleep latency showing synergic effects with muscimol (0.2 mg/kg) in shortening sleep onset and enhancing sleep time induced by pentobarbital, both at the hypnotic (40 mg/kg) and sub-hypnotic (28 mg/kg) doses. Additionally, PA elevated intracellular chloride levels in hypothalamic primary cultured neuronal cells of rats. Moreover, Western blotting quantitative results showed that PA increased the amount of protein level expression of GAD65/67 over a broader range of doses. PA increased α- and β-subunits protein levels, but decreased γ-subunit protein levels in GABAA receptors. The present experiment provides evidence for the hypnotic effects as PA enhanced pentobarbital-induced sleeping behaviors via GABAA-ergic mechanisms in rodents.
    Taken together, it is proposed that PA may be useful for the treatment of sleep disturbed subjects with insomnia.
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.8912 mL 9.4561 mL 18.9122 mL 37.8243 mL 47.2804 mL
    5 mM 0.3782 mL 1.8912 mL 3.7824 mL 7.5649 mL 9.4561 mL
    10 mM 0.1891 mL 0.9456 mL 1.8912 mL 3.7824 mL 4.728 mL
    50 mM 0.0378 mL 0.1891 mL 0.3782 mL 0.7565 mL 0.9456 mL
    100 mM 0.0189 mL 0.0946 mL 0.1891 mL 0.3782 mL 0.4728 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.
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    6α-羟基猪苓酸C; 6alpha-Hydroxypolyporenic acid C CFN92741 24513-63-1 C31H46O5 = 498.7 5mg QQ客服:1457312923
    新化合物15; New compound 15 CFN95413 N/A C31H46O6 = 514.7 5mg QQ客服:2056216494
    茯苓新酸A; Poricoic acid A(F) CFN92838 137551-38-3 C31H46O5 = 498.7 20mg QQ客服:2159513211
    茯苓酸AM; Poricoic acid AM CFN91538 151200-92-9 C32H48O5 = 512.7 5mg QQ客服:1413575084
    Poricoic acid AE ; Poricoic acid AE CFN96980 1159753-88-4 C33H50O5 = 526.75 5mg QQ客服:1457312923
    24(31)-Dehydrocarboxyacetylquercinic acid; 24(31)-Dehydrocarboxyacetylquercinic acid CFN96179 127970-62-1 C34H50O7 = 570.8 5mg QQ客服:2159513211
    齿孔酸; 齿孔菌酸; Eburicoic acid CFN90414 560-66-7 C31H50O3 = 470.73 10mg QQ客服:3257982914
    土莫酸; Tumulosic acid CFN95399 508-24-7 C31H50O4 = 486.7 5mg QQ客服:3257982914
    茯苓酸; 茯灵酸; Pachymic acid CFN99590 29070-92-6 C33H52O5 = 528.76 20mg QQ客服:2159513211
    二氢齿孔酸; Dehydroeburicoic acid CFN92740 6879-05-6 C31H48O3 = 468.7 5mg QQ客服:2056216494





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