|Source:||The rhizome of Atractylodes macrocephala Koidz.|
|Biological Activity or Inhibitors:||1. Atractylenolide III may control immunological reactions by regulating the cellular functions of IL-6 in mast cells.
2. Atractylenolide III and atractylenolide I have anti-inflammatory activity through inhibition of nuclear factor-κB and mitogen-activated protein kinase pathways in mouse macrophages, can inhibit Lipopolysaccharide-induced TNF- α and NO production in macrophages.
3. Atractylenolide III can induce apoptosis in human lung carcinoma A549 cells via mitochondria-mediated death pathway, indicates that it is a potential candidate for treatment of human lung carcinoma.
4. Atractylenolide III (LD50, 103.3 mg/m2) and atractylon (136.2 mg/m2) are potential house dust mite control agents, they are five and four times more toxic than Deet and 1.7- and 1.3-fold more active than dibutyl phthalate, respectively, based on 24 h LD50 values.
5. Atractylenolide III has neuroprotection against glutamate-induced neuronal apoptosis via inhibiting caspase signaling pathway.
6. Atractylenolide III has gastroprotective activity on ethanol-induced gastric ulcer in vitro and in vivo.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.0271 mL||20.1353 mL||40.2706 mL||80.5412 mL||100.6765 mL|
|5 mM||0.8054 mL||4.0271 mL||8.0541 mL||16.1082 mL||20.1353 mL|
|10 mM||0.4027 mL||2.0135 mL||4.0271 mL||8.0541 mL||10.0677 mL|
|50 mM||0.0805 mL||0.4027 mL||0.8054 mL||1.6108 mL||2.0135 mL|
|100 mM||0.0403 mL||0.2014 mL||0.4027 mL||0.8054 mL||1.0068 mL|
Immunopharmacol Immunotoxicol. 2016;38(2):98-102.
|Anti-inflammatory activity of atractylenolide III through inhibition of nuclear factor-κB and mitogen-activated protein kinase pathways in mouse macrophages.[Pubmed: 26667579 ]|
|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. In addition, ATL-III decreased the release of NO, TNF-α, PGE2 and IL-6 in a dose-dependent manner and showed statistically significant at concentrations of 50 μM and 100 μM as well as cyclooxygenase-2 (COX-2) expression. Furthermore, ATL-III suppressed the transcriptional activity of NF-κB. ATL-III also inhibited the activation of ERK1/2, p38 and JNK1/2 in LPS-treated macrophages and showed statistically significant at concentrations of 25 μM and 100 μM. These data suggest that ATL-III shows an anti-inflammatory effect by suppressing the release of NO, PGE2, TNF-α and IL-6 related to the NF-κB- and MAPK-signaling pathways.|
Neurochem Res. 2014 Sep;39(9):1753-8.
|Neuroprotection of atractylenolide III from Atractylodis macrocephalae against glutamate-induced neuronal apoptosis via inhibiting caspase signaling pathway.[Pubmed: 24958167]|
|Glutamate-induced excitotoxicity appears to play a crucial role in neurological disorders. Neuroprotection against glutamate-induced excitotoxicity has been proposed as a therapeutic strategy for preventing and/or treating these excitotoxicity-mediated diseases. In the present study, Atractylenolide III, which exhibited significantly neuroprotective effect against glutamate-induced neuronal apoptosis, was isolated from Atractylodes macrocephala by means of bioactivity-guided fractionation. The inhibitory effect of Atractylenolide III on glutamate-induced neuronal apoptosis was in a concentration-dependent manner. The anti-apoptotic property of Atractylenolide III might be mediated, in part, via inhibiting caspase signaling pathway. Atractylenolide III may have therapeutic potential in excitotoxicity-mediated neurological diseases.|
J Nat Prod. 2011 Feb 25;74(2):223-7.
|Blockade of IL-6 secretion pathway by the sesquiterpenoid atractylenolide III.[Pubmed: 21302967]|
|Atractylenolide III (1) is the major bioactive component of Atractylodes lancea. The aim of this study was to analyze the effect on the regulation of interleukin (IL)-6 secretion pathway caused by 1. This sesquiterpenoid inhibited the secretion and expression of IL-6 in phorbol 12-myristate 13-acetate- and calcium ionophore A23187-stimulated human mast cells (HMC)-1. In addition, 1 inhibited histamine release in stimulated HMC-1 cells. In stimulated HMC-1 cells, 1 suppressed activation of p38 mitogen-activated protein kinase, C-Jun-N-terminal protein kinase, and nuclear factor-κB. In addition, 1 suppressed the activation of caspase-1 and the expression of receptor interacting protein-2. These results provide new insights that Atractylenolide III (1) may control immunological reactions by regulating the cellular functions of IL-6 in mast cells.|
Food Chem Toxicol. 2011 Feb;49(2):514-9.
|Atractylenolide III, a sesquiterpenoid, induces apoptosis in human lung carcinoma A549 cells via mitochondria-mediated death pathway.[Pubmed: 21130827]|
|Pharmacological agents that are safe and can sensitize the lung cancer are urgently required. We investigated whether Atractylenolide III (ATL-III), the major component of Atractylodes rhizome can induce apoptosis of the lung carcinoma cells. Atractylenolide III inhibited cell growth, increased lactate dehydrogenase release and modulated cell cycle on human lung carcinoma A549 cells. Atractylenolide III induced the activation of caspase-3 and caspase-9 and cleavage of poly-(ADP)-ribose polymerase. Atractylenolide III induced the release of cytochrome c, upregulation of bax expression, and translocation of apoptosis-inducing factor. In addition, Atractylenolide III inhibited the proliferation and capillary tube formation of human umbilical vein endothelial cells. These data indicate that Atractylenolide III is a potential candidate for treatment of human lung carcinoma.|
J Pharm Pharmacol. 2010 Mar;62(3):381-8
|Gastroprotective activity of atractylenolide III from Atractylodes ovata on ethanol-induced gastric ulcer in vitro and in vivo.[Pubmed: 20487223 ]|
|Atractylon, atractylenolide I and biatractylolide were strongly toxic in PRGM cells, whilst atractylenolides II and III were not. Atractylenolide II did not show cytoprotective effects, but oral administration of Atractylenolide III dose-dependently prevented ethanol-induced PRGM cell death and cell membrane damage. The EC50 values were 0.27 and 0.34 mm, respectively. In the in-vivo assay, Atractylenolide III 10 mg/kg significantly reduced 70% ethanol-induced Wistar rat gastric ulcer. Atractylenolide III could inhibit matrix metalloproteinase (MMP)-2 and MMP-9 expression through upregulation of tissue inhibitors of metalloproteinase from the gastric ulcerated tissues. CONCLUSIONS: Atractylenolide III was the major gastroprotective component of A. ovata in ethanol-induced acute gastric ulcer. It is suggested that the gastroprotective mechanism of Atractylenolide III was via inhibition of the MMP-2 and MMP-9 pathway.|
J Agric Food Chem. 2007 Jul 25;55(15):6027-31.
|Toxicity of atractylon and atractylenolide III Identified in Atractylodes ovata rhizome to Dermatophagoides farinae and Dermatophagoides pteronyssinus.[Pubmed: 17595110]|
|In fabric-circle residual contact bioassays with adult D. farinae, Atractylenolide III (LD50, 103.3 mg/m2) and atractylon (136.2 mg/m2) were five and four times more toxic than Deet and 1.7- and 1.3-fold more active than dibutyl phthalate, respectively, based on 24 h LD50 values. These compounds were less toxic than benzyl benzoate (LD50, 45.8 mg/m2). Against adult D. pteronyssinus, Atractylenolide III (LD50, 73.8 mg/m2) and atractylon (72.1 mg/m2) were eight times more active than Deet and 2.5-fold more toxic than dibutyl phthalate. These compounds were slightly less effective than benzyl benzoate (LD50, 46.0 mg/m2). In vapor-phase toxicity tests with both mite species, Atractylenolide III and atractylon were effective in closed but not in open containers. These results indicate that the effect of these sesquiterpenoids was largely a result of action in the vapor phase. Naturally occurring Atractylenolide III and atractylon merit further study as potential house dust mite control agents or leads because of their great activity as a fumigant.|
Phytother Res. 2007 Apr;21(4):347-53.
|Atractylenolide I and atractylenolide III inhibit Lipopolysaccharide-induced TNF-alpha and NO production in macrophages.[Pubmed: 17221938]|
|Atractylenolide I and Atractylenolide III decreased the TNF-alpha level in LPS-stimulated peritoneal macrophages in a dose-dependent manner, their IC(50) values were 23.1 microm and 56.3 microm, respectively. RT-PCR analysis indicated that they inhibited TNF-alpha mRNA expression. Furthermore, they inhibited NO production in LPS-activated peritoneal macrophages, the IC(50) value of atractylenolide I was 41.0 microm, and the inhibition ratio of 100 microm of Atractylenolide III was 45.1% +/- 6.2%. The activity analysis of inducible nitric oxide synthase (iNOS) indicated that they could inhibit the activity of iNOS, their IC(50) values were 67.3 microm and 76.1 microm, respectively. Western blot analysis showed that atractylenolide I and Atractylenolide III attenuated LPS-induced synthesis of iNOS protein in the macrophages, in parallel. These results imply that the antiinflammatory mechanism of atractylenolide I and Atractylenolide III may be explained at least in part, by the inhibition of TNF-alpha and NO production. Atractylenolide I showed more potent inhibition than Atractylenolide III in the production of TNF-alpha and NO in LPS-activated peritoneal macrophages. So, atractylenolide I could be a candidate for the development of new drugs to treat inflammatory diseases accompanied by the overproduction of TNF-alpha and NO.|