Catalogue Number
BF-A2011
Analysis Method
HPLC,NMR,MS
Specification
98%
Storage
-20℃
Molecular Weight
248.32
Appearance
Off-white crystalline powder
Botanical Source
Atractylodes macrocephala
Structure Type
Terpenoids
Category
Standards;Natural Pytochemical;API
SMILES
CC1=C2CC3C(=C)CCCC3(CC2(OC1=O)O)C
Synonyms
Atractylenolide III/Naphtho(2,3-b)furan-2(4H)-one, 4a,5,6,7,8,8a,9,9a-octahydro-9a-hydroxy-3,8a-dimethyl-5-methylene-, (4aS,8aR,9aS)-/codonolactone/ATRACTYLENOLIDE/8-HYDROXYASTEROLIDE/(4aS,8aR,9aS)-9a-Hydroxy-3,8a-dimethyl-5-methylene-4a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2(4H)-one/Naphtho[2,3-b]furan-2(4H)-one, 4a,5,6,7,8,8a,9,9a-octahydro-9a-hydroxy-3,8a-dimethyl-5-methylene-, (4aS,8aR,9aS)-
IUPAC Name
(4aS,8aR,9aS)-9a-hydroxy-3,8a-dimethyl-5-methylidene-4,4a,6,7,8,9-hexahydrobenzo[f][1]benzofuran-2-one
Density
1.2±0.1 g/cm3
Solubility
Methanol; Acetontrile; DMSO
Flash Point
181.1±21.5 °C
Boiling Point
424.6±45.0 °C at 760 mmHg
Melting Point
200-201ºC
InChl
InChl Key
FBMORZZOJSDNRQ-GLQYFDAESA-N
WGK Germany
RID/ADR
HS Code Reference
2932990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:73030-71-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
COA
31178951
Oxidative stress contributes to muscle wasting in advanced chronic kidney disease (CKD) patients. Atractylenolide III (ATL-III), the major active constituent of Atractylodes rhizome, has been previously reported to function as an antioxidant. This study is aimed at investigating whether ATL-III has protective effects against CKD-induced muscle wasting by alleviating oxidative stress. The results showed that the levels of serum creatinine (SCr), blood urea nitrogen (BUN), and urinary protein significantly decreased in the ATL-III treatment group compared with the 5/6 nephrectomy (5/6 Nx) model group but were higher than those in the sham operation group. Skeletal muscle weight was increased, while inflammation was alleviated in the ATL-III administration group compared with the 5/6 Nx model group. ATL-III-treated rats also showed reduced dilation of the mitochondria, increased CAT, GSH-Px, and SOD activity, and decreased levels of MDA both in skeletal muscles and serum compared with 5/6 Nx model rats, suggesting that ATL-III alleviated mitochondrial damage and increased the activity of antioxidant enzymes, thus reducing the production of ROS. Furthermore, accumulated autophagosomes (APs) and autolysosomes (ALs) were reduced in the gastrocnemius (Gastroc) muscles of ATL-III-treated rats under transmission electron microscopy (TEM) together with the downregulation of LC3-II and upregulation of p62 according to Western blotting. This evidence indicated that ATL-III improved skeletal muscle atrophy and alleviated oxidative stress and autophagy in CKD rats. Furthermore, ATL-III could also increase the protein levels of p-PI3K, p-AKT, and p-mTOR in skeletal muscles in CKD rats. To further reveal the relevant mechanism, the oxidative stress-mediated PI3K/AKT/mTOR pathway was assessed, which showed that a reduced expression of p-PI3K, p-AKT, and p-mTOR in C2C12 myoblast atrophy induced by TNF-α could be upregulated by ATL-III; however, after the overexpression of Nox2 to increase ROS production, the attenuated effect was reversed. Our findings indicated that ATL-III is a potentially protective drug against muscle wasting via activation of the oxidative stress-mediated PI3K/AKT/mTOR pathway.
Atractylenolide III Attenuates Muscle Wasting in Chronic Kidney Disease via the Oxidative Stress-Mediated PI3K/AKT/mTOR Pathway.
Wang M1,2, Hu R1,2, Wang Y3, Liu L1,2, You H1,2, Zhang J2, Wu X1,2, Pei T2, Wang F2, Lu L4, Xiao W2, Wei L1,2.
2019 Apr 18
32196713
Pediatric asthma is a common inflammatory disease in children. Atractylenolide III is an active component of the Atractylodes rhizome, an herbal medicine that has been used as an asthma treatment. This study aimed to explore the effects and underlying mechanisms of atractylenolide III in IL-4-induced 16HBE cells and ovalbumin induced asthmatic mice. The results showed that IL-4 stimulation significantly decreased, and atractylenolide III treatment increased, growth and apoptosis of 16HBE cells. In 16HBE cells, administration of atractylenolide III also significantly suppressed the IL-4-induced increases in the expression of cleaved caspase-1; apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC); and nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3). Moreover, the numbers of total leukocytes, neutrophils, eosinophils, and macrophages significantly increased in ovalbumin-induced mice, and then decreased after atractylenolide III treatment. In ovalbumin-induced asthmatic mice, atractylenolide III treatment also significantly inhibited NLRP3 inflammasome activation and restored the Th1/Th2 balance. These results indicate that atractylenolide III reduced NLRP3 inflammasome activation and regulated the Th1/Th2 balance in IL-4 induced 16HBE cells and ovalbumin-induced asthmatic mice, suggesting it has a protective effect that may be useful in the treatment of pediatric asthma.
This article is protected by copyright. All rights reserved.
16HBE; NLRP3; Th1/Th2; atractylenolide III; pediatric asthma
Atractylenolide III reduces NLRP3 inflammasome activation and Th1/Th2 imbalances in both in vitro and in vivo models of asthma.
Zhu C1, Zhang L2, Liu Z1, Li C1, Bai Y1, Wang L1.
2020 Mar 20
31679309
BACKGROUND:
Natural active components have been reported to serve as adjuvant medications in the clinical practice of cancer therapeutics. However, the antineoplastic roles of atractylenolide III (ATL) are rarely reported. In the present study, we assessed the functions of ATL combined with docetaxel in gastric cancer cells.
METHODS:
Cell viability and cytotoxic activity were evaluated using CCK-8 and LDH-based cytotoxicity assays, respectively. Protein expression levels were measured by western blotting analysis. Annexin V-FITC/PI staining was used to evaluate cell apoptosis using flow cytometry.
RESULTS:
AGS and SGC-7901 cell viability was significantly inhibited in ATL combined with docetaxel group compared with docetaxel treatment alone. The levels of LDH, apoptosis rate, and the ratio of BAX to Bcl-2 were significantly elevated in combination treatment group compared to docetaxel treatment alone. Intriguingly, docetaxel combined with ATL resulted in a significant decrease in FGFR1, FGFR2, and FGFR4 protein expression compared with docetaxel treatment alone. Knockout of FGFR1, -2, and -4 exhibited a similar role of medications to inhibit growth and induce apoptosis in AGS and SGC-7901 cells.
CONCLUSIONS:
ATL and docetaxel treatment performed the synergistic effects on the inhibition of growth and induction of apoptosis in gastric cancer cells, and the underlying mechanism was mediated, at least partially, through the inhibition of FGFR1, -2, and -4.
Atractylenolide III Enhances the Anti-Neoplastic Efficacy of Docetaxel in Gastric Cancer Cell by Inhibiting Fibroblast Growth Factor Receptors 1, -2, and -4 Expression.
Ji Y1, Kang Z1, Kang N2, Zhao Y1, Guo Q1, Chen Y1.
2019
