Atractylenolide III - CAS 73030-71-4
Catalog number: 73030-71-4
Category: Inhibitor
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Molecular Formula:
C15H20O3
Molecular Weight:
248.32
COA:
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Targets:
Others
Description:
Atractylenolide III is a major component of Atractylodes rhizome, which can induce apoptosis of the lung carcinoma cells.
Purity:
>98%
Synonyms:
Codonolactone; 8β-Hydroxyasterolide
MSDS:
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InChIKey:
FBMORZZOJSDNRQ-GLQYFDAESA-N
InChI:
InChI=1S/C15H20O3/c1-9-5-4-6-14(3)8-15(17)12(7-11(9)14)10(2)13(16)18-15/h11,17H,1,4-8H2,2-3H3/t11-,14+,15-/m0/s1
Canonical SMILES:
CC1=C2CC3C(=C)CCCC3(CC2(OC1=O)O)C
1.A systems pharmacology approach to decipher the mechanism of danggui-shaoyao-san decoction for the treatment of neurodegenerative diseases.
Luo Y1, Wang Q2, Zhang Y3. J Ethnopharmacol. 2016 Feb 3;178:66-81. doi: 10.1016/j.jep.2015.12.011. Epub 2015 Dec 8.
ETHNOPHARMACOLOGICAL RELEVANCE: Neurodegenerative diseases (NDs) is a time-dependent course for a sequence of conditions that primarily impact the neurons in the human brain, ultimately, resulting in persistence and progressive degeneration and / or death of nerve cells and reduction of cognition and memory function. Currently, there are no therapeutic approaches to cure neurodegeneration, except certain medicines that temporarily alleviate symptoms, facilitating the improvement of a patients' quality of life. Danggui-shaoyao-san (DSS), as a famous Chinese herbal formula, has been widely used in the treatment of various illnesses, including neurodegenerative diseases. Although well-practiced in clinical medicine, the mechanisms involved in DSS for the treatment of neurodegenerative diseases remain elusive.
2.Anti-inflammatory activity of atractylenolide III through inhibition of nuclear factor-κB and mitogen-activated protein kinase pathways in mouse macrophages.
Ji GQ1, Chen RQ2, Wang L3. Immunopharmacol Immunotoxicol. 2016 Apr;38(2):98-102. doi: 10.3109/08923973.2015.1122617. Epub 2015 Dec 15.
To elucidate the anti-inflammatory mechanisms involved, we investigated the effects of atractylenolide III (ATL-III) on cytokine expression, extracellular signal-regulated kinases 1 and 2 (ERK1/2), p38 mitogen-activated protein kinase (p38), C-Jun-N-terminal protein kinase1/2 (JNK1/2) and nuclear factor-κB (NF-κB) pathways in lipopolysaccharide (LPS)-induced RAW264.7 mouse macrophages. Macrophages were incubated with various concentrations (0, 25, 50, 100 μM) of ATL-III and/or LPS (1 μg/mL) for 24 h. The production of nitric oxide (NO) was determined by the Greiss reagent. The production of tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE2) and interleukin 6 (IL-6) was determined by enzyme-linked immunosorbent assay (ELISA). Furthermore, macrophages were treated with ATL-III (0, 25, 100 μM) for 1 h and then stimulated by LPS. NF-κB, p38, JNK1/2 and ERK1/2 were determined by western blotting. We found ATL-III showed no inhibitory effect on cell proliferation at concentrations ranging from 1 μM to 100 μM.
3.Anti-inflammatory activity of atractylenolide III through inhibition of nuclear factor-κB and mitogen-activated protein kinase pathways in mouse macrophages.
Ji GQ1, Chen RQ2, Wang L3. Immunopharmacol Immunotoxicol. 2016 Apr;38(2):98-102. doi: 10.3109/08923973.2015.1122617. Epub 2015 Dec 15.
To elucidate the anti-inflammatory mechanisms involved, we investigated the effects of atractylenolide III (ATL-III) on cytokine expression, extracellular signal-regulated kinases 1 and 2 (ERK1/2), p38 mitogen-activated protein kinase (p38), C-Jun-N-terminal protein kinase1/2 (JNK1/2) and nuclear factor-κB (NF-κB) pathways in lipopolysaccharide (LPS)-induced RAW264.7 mouse macrophages. Macrophages were incubated with various concentrations (0, 25, 50, 100 μM) of ATL-III and/or LPS (1 μg/mL) for 24 h. The production of nitric oxide (NO) was determined by the Greiss reagent. The production of tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE2) and interleukin 6 (IL-6) was determined by enzyme-linked immunosorbent assay (ELISA). Furthermore, macrophages were treated with ATL-III (0, 25, 100 μM) for 1 h and then stimulated by LPS. NF-κB, p38, JNK1/2 and ERK1/2 were determined by western blotting. We found ATL-III showed no inhibitory effect on cell proliferation at concentrations ranging from 1 μM to 100 μM.
4.Simultaneous determination and pharmacokinetic study of Atractylenolide I, II and III in rat plasma after intragastric administration of Baizhufuling extract and Atractylodis extract by UPLC-MS/MS.
Yan H1, Sun Y1, Zhang Q1, Yang M1, Wang X1, Wang Y1, Yu Z2, Zhao Y3. J Chromatogr B Analyt Technol Biomed Life Sci. 2015 Jul 1;993-994:86-92. doi: 10.1016/j.jchromb.2015.05.006. Epub 2015 May 14.
A simple and rapid ultra high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was developed for the simultaneous determination of Atractylenolide I, II and III in rat plasma. Plasma samples were processed by liquid-liquid extraction with ethyl acetate, using schisandrin as internal standard (IS). Chromatographic separation was accomplished on a Thermo Hypersil GOLD C18 column (2.1mm×50mm, 1.9μm) with mobile phase consisting of acetonitrile and 0.1% formic acid-water (50:50, v/v). The detection was carried out by ESI-MS (positive ionization mode) and low-energy collision dissociation tandem mass spectrometric analyses using the multiple-reaction monitoring (MRM) scan mode. The quantification was performed using the transitions of the protonated molecule→product ion at m/z 231.0→185.1 for Atractylenolide I, at m/z 233.1→187.1 for Atractylenolide II and at m/z 249.1→231.1 for Atractylenolide III, respectively.
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CAS 73030-71-4 Atractylenolide III

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