Atractylenolide ICAS# 73069-13-3 |
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 73069-13-3 | SDF | Download SDF |
| PubChem ID | 5321018 | Appearance | White powder |
| Formula | C15H18O2 | M.Wt | 230.30 |
| Type of Compound | Sesquiterpenoids | Storage | Desiccate at -20°C |
| Solubility | DMSO : 100 mg/mL (434.22 mM; Need ultrasonic) | ||
| Chemical Name | (4aS,8aS)-3,8a-dimethyl-5-methylidene-4a,6,7,8-tetrahydro-4H-benzo[f][1]benzofuran-2-one | ||
| SMILES | CC1=C2CC3C(=C)CCCC3(C=C2OC1=O)C | ||
| Standard InChIKey | ZTVSGQPHMUYCRS-SWLSCSKDSA-N | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| 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 | Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells.[Pubmed: 25270720]Immunopharmacol Immunotoxicol. 2014 Dec;36(6):420-5.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. Atractylenolide-I sensitizes human ovarian cancer cells to paclitaxel by blocking activation of TLR4/MyD88-dependent pathway.[Pubmed: 24452475]Sci Rep. 2014 Jan 23;4:3840.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.
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| In vivo | The protective effect of atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture.[Pubmed: 25853971]Pharm Biol. 2015 Apr 8:1-5.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. |
| Cell Research | Pro-oxidant and cytotoxic activities of atractylenolide I in human promyeloleukemic HL-60 cells.[Pubmed: 16624472 ]Anti-tumor effects of atractylenolide I isolated from Atractylodes macrocephala in human lung carcinoma cell lines.[Pubmed: 24172243]Molecules. 2013 Oct 29;18(11):13357-68.Atractylenolide I (ATL-1) is the major sesquiterpenoid of Atractylodes macrocephala. This study was designed to investigate whether Atractylenolide I induced apoptosis in A549 and HCC827 cells in vitro and in vivo.
Food Chem Toxicol. 2006 Aug;44(8):1308-15.The dried rhizome of Bai Zhu (Atractylodes ovata) is widely used as a Chinese herbal medicine. Two sesquiterpenolides of similar structures (Atractylenolide I, AT-I; Atractylenolide III, AT-III) were isolated from dried rhizome of Atractylodes ovata.
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| Animal Research | Inhibitory effect of atractylenolide I on angiogenesis in chronic inflammation in vivo and in vitro.[Pubmed: 19356732]Eur J Pharmacol. 2009 Jun 10;612(1-3):143-52.Angiogenesis is involved in the pathology of chronic inflammatory diseases. Application of anti-angiogenic strategies is beneficial in the treatment of inflammatory disorders. Atractylenolide I is an anti-inflammation agent.
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Atractylenolide I Dilution Calculator
Atractylenolide I Molarity Calculator
| 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 necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Atractylenolide I is a natural compound extracted from largehead atractylodes rhizome; induce apoptosis and bring about cytotoxicity of human promyeloleukemic HL-60 cells; TLR4-antagonizing agent. IC50 value: Target: TLR4 antagonist in vitro: The ID(50) values of atractylenolide I were 15.15 mg/kg and 3.89 microg/ml for inhibiting the vascular index in vivo and microvessel outgrowth in vitro, respectively. Atractylenolide I could dose-dependently inhibit the production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) activity in the flute of mouse air pouch and the peritoneal macrophages stimulated by lipopolysaccharide (LPS) [1]. ATL-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, ATL-I suppressed the activity of nuclear NF-κB and the phosphorylation of ERK1/2 and p38 in LPS-treated RAW264.7 cells [2]. AT-I inhibited the self-renewal capacity of gastric stem-like cells (GCSLCs) by suppression of their sphere formation capacity and cell viability. AT-I attenuated gastric cancer stem cell (GCSC) traits partly through inactivating Notch1, leading to reducing the expressions of its downstream target Hes1, Hey1 and CD44 in vitro [3]. 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 [4]. in vivo: In the in vivo study, ATL-I effectively suppressed tumor growth (A549) in transplanted tumor nude mice with up-regulation of caspase-3, caspase-9, and Bax and down-regulation of Bcl-2 and Bcl-XL [5].
References:
[1]. Wang C, et al. Inhibitory effect of atractylenolide I on angiogenesis in chronic inflammation in vivo and in vitro. Eur J Pharmacol. 2009 Jun 10;612(1-3):143-52.
[2]. Ji G, et al. Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells. Immunopharmacol Immunotoxicol. 2014 Dec;36(6):420-5.
[3]. Ma L, et al. Atractylenolide I-mediated Notch pathway inhibition attenuates gastric cancer stem cell traits. Biochem Biophys Res Commun. 2014 Jul 18;450(1):353-9.
[4]. Huang JM, et al. Atractylenolide-I sensitizes human ovarian cancer cells to paclitaxel by blocking activation of TLR4/MyD88-dependent pathway. Sci Rep. 2014 Jan 23;4:3840.
[5]. Liu H, et al. Anti-tumor effects of atractylenolide I isolated from Atractylodes macrocephala in human lung carcinoma cell lines. Molecules. 2013 Oct 29;18(11):13357-68.
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Anti-tumor effects of atractylenolide I isolated from Atractylodes macrocephala in human lung carcinoma cell lines.[Pubmed:24172243]
Molecules. 2013 Oct 29;18(11):13357-68.
Atractylenolide I (ATL-1) is the major sesquiterpenoid of Atractylodes macrocephala. This study was designed to investigate whether ATL-1 induced apoptosis in A549 and HCC827 cells in vitro and in vivo. In our results, ATL-1 significantly decreased the percentage of in vitro viability, in a dose-dependent manner. In addition, DAPI staining and flow cytometry tests demonstrated the induction of apoptosis by ATL-I. Western blot analysis indicated that the protein levels of caspase-3, caspase-9 and Bax were increased in A549 and HCC827 cells after ATL-I exposure; to the contrary, the expressions of Bcl-2, Bcl-XL were decreased after treatment with ATL-1. In the in vivo study, ATL-I effectively suppressed tumor growth (A549) in transplanted tumor nude mice with up-regulation of caspase-3, caspase-9, and Bax and down-regulation of Bcl-2 and Bcl-XL. In conclusion, our results demonstrated that ATL-I has significant antitumor activity in lung carcinoma cells, and the possible mechanism of action may be related to apoptosis induced by ATL-I via a mitochondria-mediated apoptosis pathway.
The protective effect of atractylenolide I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture.[Pubmed:25853971]
Pharm Biol. 2016;54(1):146-50.
CONTEXT: Atractylenolide I (AT-I), an active compound isolated from Atractylodes macrocephala Koidz (Compositae), shows several pharmacological activities. OBJECTIVE: Our present study is designed to investigate the protective effect of AT-I on systemic inflammation in the mouse model of sepsis created by cecal ligation and puncture (CLP), and explore the possible mechanism. MATERIALS AND METHODS: Sepsis mouse model was established by CLP, and the tested dosages of AT-I were 10, 20, and 40 mg/kg (ip). Pro-inflammatory cytokines in serum (TNF-alpha, IL-1beta 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. RESULTS: Our results indicated that AT-I significantly increased the survival rate of mice with sepsis (p < 0.05), whereas the WBCs and levels of LPS, pro-inflammatory cytokines (TNF-alpha, IL-1beta and IL-6), ALT, AST, Cre, and BUN decreased significantly after treatment with AT-I (p < 0.05). CONCLUSION: In conclusion, the AT-I ameliorates sepsis syndrome by reduction of pro-inflammatory cytokines and LPS, and provides an improvement in liver and kidney functions.
Pro-oxidant and cytotoxic activities of atractylenolide I in human promyeloleukemic HL-60 cells.[Pubmed:16624472]
Food Chem Toxicol. 2006 Aug;44(8):1308-15.
The dried rhizome of Bai Zhu (Atractylodes ovata) is widely used as a Chinese herbal medicine. Two sesquiterpenolides of similar structures (Atractylenolide I, AT-I; Atractylenolide III, AT-III) were isolated from dried rhizome of Atractylodes ovata. Incubation of AT-I with recombinant human Cu,Zn-superoxide dismutase (rhCu,Zn-SOD) resulted in rhCu,Zn-SOD fragmentations and Zn releases. However, these were not observed in the AT-III reaction. The AT-1 showed dose-dependent cytotoxic activities (7.5, 15, and 30 microg/ml) on the human promyeloleukemic HL-60 cells while AT-III did not, and the IC50 of the former being 10.6 microg/ml (corresponding to 46 microM) on 12 h-treated cells. The results of DNA ladder and DNA contents in sub-G1 type revealed that AT-I induced apoptosis in human promyeloleukemic HL-60 cells. The cytotoxic and pharmacological mechanisms of AT-I against human promyeloleukemic HL-60 cells was investigated. The AT-I appeared to exhibit both pro-oxidant and antioxidant properties after an ESR spectrometer was used to detect hydroxyl radical productions in vitro and flow cytometry to detect intracellular ROS productions in AT-I treated cells. The AT-1 also showed dose-dependent Cu,Zn-SOD inhibitory activity in HL-60 cells treated for 12 h, confirmed by activity and immune stainings. However, catalase, Mn-SOD, and glutathione peroxidase did not apparently change activities under the same treatments. The addition of commercial rhCu,Zn-SOD (25-100 U/mL) to the AT-I-treated HL-60 cells (15 microg/ml) resulted in significant differences (p<0.01) and could reduce the AT-I cytotoxicity from 78% to 28% on HL-60 cells. It was proposed that the AT-I might work via Cu,Zn-SOD inhibition in HL-60 cells to induce apoptosis and bring about cytotoxicity.
Inhibitory effect of atractylenolide I on angiogenesis in chronic inflammation in vivo and in vitro.[Pubmed:19356732]
Eur J Pharmacol. 2009 Jun 10;612(1-3):143-52.
Angiogenesis is involved in the pathology of chronic inflammatory diseases. Application of anti-angiogenic strategies is beneficial in the treatment of inflammatory disorders. Atractylenolide I is an anti-inflammation agent. To further investigate the anti-angiogenesis mechanism of Atractylenolide I in cell and mice based on inflammation model, the vascular index and microvessel outgrowth were measured by using the Freunds complete adjuvant (FCA) induced mouse air pouch model as well as the mice aortic ring co-cultured with peritoneal macrophages model. The ID(50) values of Atractylenolide I were 15.15 mg/kg and 3.89 microg/ml for inhibiting the vascular index in vivo and microvessel outgrowth in vitro, respectively. Atractylenolide I could dose-dependently inhibit the production of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) activity in the flute of mouse air pouch and the peritoneal macrophages stimulated by lipopolysaccharide (LPS). Atractylenolide I displayed a potent inhibitory effect on angiogenesis by a set of down-regulatory actions of NO, TNF-alpha, IL-1beta, IL-6, VEGF and PlGF in chronic inflammation.
Atractylenolide I inhibits lipopolysaccharide-induced inflammatory responses via mitogen-activated protein kinase pathways in RAW264.7 cells.[Pubmed:25270720]
Immunopharmacol Immunotoxicol. 2014 Dec;36(6):420-5.
Atractylenolide I (ATL-I) is a bioactive component of Rhizoma Atractylodis macrocephalae. Although increasing evidence shows that ATL-I has an anti-inflammatory effect, the anti-inflammatory molecular mechanism of ATL-I is still unknown. In this study, we investigated the effect of ATL-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-alpha) by enzyme-linked immunosorbent assay (ELISA) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Further, we examined the effect of ATL-I on the activation of nuclear factor-kappaB (NF-kappaB) 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 ATL-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 ATL-I showed no inhibitory effect on cell viability at concentrations ranging from 1 microM to 100 microM and markedly reduced the release of IL-6 and TNF-alpha at a concentrate-dependent manner. In addition, ATL-I suppressed the activity of nuclear NF-kappaB 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. These data suggest that ATL-I shows an anti-inflammatory effect by inhibiting TNF-alpha and IL-6 production. The anti-inflammatory effects of ATL-I may be associated with the inhibition of the NF-kappaB, ERK1/2 and p38 signaling pathways.
Atractylenolide-I sensitizes human ovarian cancer cells to paclitaxel by blocking activation of TLR4/MyD88-dependent pathway.[Pubmed:24452475]
Sci Rep. 2014 Jan 23;4:3840.
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. 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. 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-kappaB pathway.
