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  • 白术内酯I; 苍术内酯I

    Atractylenolide I

    白术内酯I; 苍术内酯I
    产品编号 CFN99944
    CAS编号 73069-13-3
    分子式 = 分子量 C15H18O2 = 230.30
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Sesquiterpenoids
    植物来源 The rhizomes of Atractylodes macrocephala Koidz.
    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
    白术内酯I; 苍术内酯I CFN99944 73069-13-3 10mg QQ客服:1457312923
    白术内酯I; 苍术内酯I CFN99944 73069-13-3 20mg QQ客服:1457312923
    白术内酯I; 苍术内酯I CFN99944 73069-13-3 50mg QQ客服:1457312923
    白术内酯I; 苍术内酯I CFN99944 73069-13-3 100mg QQ客服:1457312923
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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
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  • Molecules.2018, 23(7):E1817
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  • Eur J Pharmacol.2021, 899:174010.
  • Molecules2020, 25(4):892
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  • Evid Based Complement Alternat Med.2018, 2018:4259603
  • Life Sci.2018, 209:498-506
  • JEJU National University2022, 10478.
  • J Health Sci Med Res.2023, 31584.
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  • ...
  • 生物活性
    Description: Atractylenolide I, a TLR4-antagonizing agent, shows a wide spectrum of pharmacological activities such as anti-inflammatory, digestion promoting,significant antitumor, and antioxidant effects. It ameliorates sepsis syndrome,liver and kidney functions by reduction of pro-inflammatory cytokines and LPS.
    Targets: TNF-α | IL Receptor | ERK | p38MAPK | TLR | NF-kB | Bcl-2/Bax | Caspase | NO | VEGFR
    In vitro:
    Immunopharmacol Immunotoxicol. 2014 Dec;36(6):420-5.
    Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells.[Pubmed: 25270720]
    Atractylenolide I (ATL-I) is a bioactive component of Rhizoma Atractylodis macrocephalae. Although increasing evidence shows that Atractylenolide I has an anti-inflammatory effect, the anti-inflammatory molecular mechanism of Atractylenolide I is still unknown.
    METHODS AND RESULTS:
    In this study, we investigated the effect of Atractylenolide I on cell viability by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and the level of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) by enzyme-linked immunosorbent assay (ELISA) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Further, we examined the effect of Atractylenolide I on the activation of nuclear factor-kappaB (NF-κB) and phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (p38) by Western blot. We also investigated the effect of Atractylenolide I on the expression of myeloid differentiation protein-2 (MD-2), CD14, complement receptor 3 (CR3), scavenger receptor class A (SR-A), toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). We found that Atractylenolide I showed no inhibitory effect on cell viability at concentrations ranging from 1 μM to 100 μM and markedly reduced the release of IL-6 and TNF-α at a concentrate-dependent manner. In addition, Atractylenolide I suppressed the activity of nuclear NF-κB and the phosphorylation of ERK1/2 and p38 in LPS-treated RAW264.7 cells. Further analysis showed that ATL-I inhibited the expression of MD-2, CD14, SR-A, TLR4 and MyD88, but the expression of CR3 was unaffected.
    METHODS AND RESULTS:
    These data suggest that Atractylenolide I shows an anti-inflammatory effect by inhibiting TNF-α and IL-6 production. The anti-inflammatory effects of Atractylenolide I may be associated with the inhibition of the NF-κB, ERK1/2 and p38 signaling pathways.
    Sci Rep. 2014 Jan 23;4:3840.
    Atractylenolide-I sensitizes human ovarian cancer cells to paclitaxel by blocking activation of TLR4/MyD88-dependent pathway.[Pubmed: 24452475]
    Paclitaxel, a known TLR4 ligand, leads to activation of TLR4/MyD88-dependent pathway that mediates chemoresistance and tumor progression in epithelial ovarian carcinoma (EOC). Atractylenolide I (AO-I), a novel TLR4-antagonizing agent, inhibits TLR4 signaling by interfering with the binding of LPS or paclitaxel to membrane TLR4 of human leukocytes.
    METHODS AND RESULTS:
    In this study, AO-I was found to attenuate paclitaxel-induced protein expression of IL-6, VEGF and survivin, and to enhance early apoptosis and growth inhibition in MyD88(+) EOC cells; AO-I was shown to fit into the hydrophobic pocket of human MD-2 and to partially overlap with the binding site of paclitaxel by docking simulations, suggesting that AO-I may block the MD-2-mediated TLR4/MyD88-dependent paclitaxel signaling in MyD88(+) EOC cells.
    CONCLUSIONS:
    Therefore, AO-I could significantly sensitize the response of MyD88(+) EOC cells to paclitaxel by blocking MD-2-mediated TLR4/MyD88 signaling, and that AO-I-paclitaxel combination could be a promising strategy for the treatment of EOC with a functional TLR4/MyD88/NF-κB pathway.
    Exp Dermatol . 2018 Feb;27(2):201-204.
    The JAK2/STAT3 pathway is involved in the anti-melanoma effects of atractylenolide I[Pubmed: 29078004]
    Abstract In this study, we aimed to investigate the anti-melanoma effects and the JAK2/STAT3 pathway-related mechanism of action of atractylenolide I in human melanoma cells. Our results showed that atractylenolide I effectively reduced viability, induced apoptosis and inhibited migration of melanoma cells. Meanwhile, atractylenolide I decreased the protein expression levels of phospho-JAK2 and phospho-STAT3, and in turn downregulated the mRNA levels of STAT3-targeted genes, including Bcl-xL, MMP-2 and MMP-9. Furthermore, the cytotoxic effect of atractylenolide I was attenuated in STAT3-overactivated A375 cells. These findings indicate that inhibition of JAK2/STAT3 signalling contributes to the anti-melanoma effects of atractylenolide I.
    Exp Cell Res . 2017 Apr 1;353(1):26-34.
    Atractylenolide I restores HO-1 expression and inhibits Ox-LDL-induced VSMCs proliferation, migration and inflammatory responses in vitro[Pubmed: 28274716]
    Abstract Pathogenesis of atherosclerosis is characterized by the proliferation and migration of vascular smooth muscle cells (VSMCs) and inflammatory lesions. The aim of this study is to elucidate the effect of atractylenolide I (AO-I) on smooth muscle cell inflammation, proliferation and migration induced by oxidized modified low density lipoprotein (Ox-LDL). Here, We found that atractylenolide I inhibited Ox-LDL-induced VSMCs proliferation and migration in a dose-dependent manner, and decreased the production of inflammatory cytokines and the expression of monocyte chemoattractant protein-1 (MCP-1) in VSMCs. The study also identified that AO-I prominently inhibited p38-MAPK and NF-κB activation. More importantly, the specific heme oxygenase-1 (HO-1) inhibitor zinc protoporphyrin (ZnPP) IX partially abolished the beneficial effects of atractylenolide I on Ox-LDL-induced VSMCs. Furthermore, atractylenolide I blocked the foam cell formation in macrophages induced by Ox-LDL. In summary, inhibitory roles of AO-I in VSMCs proliferation and migration, lipid peroxidation and subsequent inflammatory responses might contribute to the anti-atherosclerotic property of AO-I. Keywords: Atherosclerosis; Atractylenolide I; Inflammation; Migration; Proliferation; Vascular smooth muscle cells.
    In vivo:
    Pharm Biol. 2015 Apr 8:1-5.
    The protective effect of atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture.[Pubmed: 25853971]
    Atractylenolide I (AT-I), an active compound isolated from Atractylodes macrocephala Koidz (Compositae), shows several pharmacological activities. Our present study is designed to investigate the protective effect of Atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture (CLP), and explore the possible mechanism.
    METHODS AND RESULTS:
    Sepsis mouse model was established by CLP, and the tested dosages of Atractylenolide I were 10, 20, and 40 mg/kg (ip). Pro-inflammatory cytokines in serum (TNF-α, IL-1β and IL-6) were determined by the ELISA method; serum lipopolysaccharide (LPS) level was measured by the Limulus Amebocyte Lysate (LAL) test; white blood cells (WBC) were counted by Blood cell analyzer; contents of alanine transaminase (ALT), aspartate transarninase (AST), creatinine (Cre), and blood urea nitrogen (BUN) in serum were determined by automatic biochemistry analyzer. For survival rate tests, CLP mice were observed within 7 days, and body temperature was measured at 0, 4, 8, 12, 24, 48 and 72 h after surgery. Our results indicated that Atractylenolide I significantly increased the survival rate of mice with sepsis (p < 0.05), whereas the WBCs and levels of LPS, pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), ALT, AST, Cre, and BUN decreased significantly after treatment with Atractylenolide I (p < 0.05).
    CONCLUSIONS:
    In conclusion, the Atractylenolide I ameliorates sepsis syndrome by reduction of pro-inflammatory cytokines and LPS, and provides an improvement in liver and kidney functions.
    Exp Ther Med . 2018 Feb;15(2):1574-1579.
    Anti-depressant-like effect of atractylenolide I in a mouse model of depression induced by chronic unpredictable mild stress[Pubmed: 29434743]
    Abstract Atractylenolide I (AT-I), a major component of the rhizoma of Atractylodes macrocephala Koidz., exerts a wide range of activities. The purpose of the present study was to investigate the anti-depressant-like effect of AT-I in a mouse model of chronic unpredictable mild stress (CUMS), and to explore the possible molecular mechanism involved. It was revealed that AT-I significantly ameliorated CUMS-induced depressive-like behaviors, as evidenced by increased sucrose preference as well as shortened immobility time in the forced swimming and the tail suspension test. In addition, AT-I reduced CUMS-induced decreases in the concentrations of serotonin and norepinephrine in the hippocampus. Furthermore, AT-I inhibited the activation of the nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome as well as the concentration of the pro-inflammatory cytokine interleukin (IL)-1β in the hippocampi of mice subjected to CUMS. In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production. Keywords: atractylenolide I; depression; inflammation; interleukin-1β; nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.3422 mL 21.7108 mL 43.4216 mL 86.8432 mL 108.5541 mL
    5 mM 0.8684 mL 4.3422 mL 8.6843 mL 17.3686 mL 21.7108 mL
    10 mM 0.4342 mL 2.1711 mL 4.3422 mL 8.6843 mL 10.8554 mL
    50 mM 0.0868 mL 0.4342 mL 0.8684 mL 1.7369 mL 2.1711 mL
    100 mM 0.0434 mL 0.2171 mL 0.4342 mL 0.8684 mL 1.0855 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
    4,8-二羟基桉叶-7(11)-烯-12,8-内酯; 4,8-Dihydroxyeudesm-7(11)-en-12,8-olide CFN99348 1231208-53-9 C15H22O4 = 266.3 5mg QQ客服:2056216494
    白术内酯I; 苍术内酯I; Atractylenolide I CFN99944 73069-13-3 C15H18O2 = 230.30 20mg QQ客服:215959384
    白术内酯II; 苍术内酯II; Atractylenolide II CFN99945 73069-14-4 C15H20O2 = 232.32 20mg QQ客服:1413575084
    白术内酯III; 苍术内酯III; Atractylenolide III CFN99946 73030-71-4 C15H20O3 = 248.32 20mg QQ客服:2159513211
    羟基香樟内脂; Hydroxylinderstrenolide CFN91529 20267-92-9 C15H18O3 = 246.3 5mg QQ客服:1457312923
    双白术内酯; Biatractylolide CFN95205 182426-37-5 C30H38O4 = 462.6 10mg QQ客服:2159513211
    8beta-Methoxyatractylenolide I; 8beta-Methoxyatractylenolide I CFN89314 193694-24-5 C16H22O3 = 262.34 5mg QQ客服:1457312923
    芹烷二烯酮; Selina-4(15),7(11)-dien-8-one CFN95078 54707-47-0 C15H22O = 218.3 10mg QQ客服:2159513211
    Chlorantholide A; Chlorantholide A CFN97968 1372558-33-2 C15H16O3 = 244.3 5mg QQ客服:2159513211
    Chlorantholide B; Chlorantholide B CFN97967 1372558-34-3 C15H18O3 = 246.3 5mg QQ客服:1457312923

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