Off-white crystalline powder
(4aS,8aR,9aS)-3,8a-dimethyl-5-methylidene-4a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2(4H)-one/AtractylenolideII/(4aS,8aR,9aS)-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-3,8a-dimethyl-5-methylene-, (4aS,8aR,9aS)-/(4aS,8aR,9aS)-4a,5,6,7,8,8a,9,9a-Octahydro-3,8a-dimethyl-5-methylenenaphtho[2,3-b]furan-2(4H)-one/Eudesmanolide/ASTEROLIDE/Atractylon-Autoxidationsprodukt A/Atractylenolide II
Methanol; Acetontrile; DMSO
378.0±41.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:73069-14-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Prostate cancer is the most common illness affecting men worldwide. Although much progress has been made in the study of prostate cancer prevention and treatment, less attention has been paid to the molecular mechanism of the disease. The molecular arrangement by which atractylenolide II (ATR II) induces human prostate cancer cytotoxicity was comprehensively examined in the present study. As indicated by the results, ATR II could inhibit prostate cancer cell proliferation and promote DU145 and LNCaP cell apoptosis through induced G2/M cell cycle arrest. The cell apoptosis process induced by ATR II in both DU145 and LNCaP cells was associated with its ability to inhibit androgen receptor (AR) with overexpression of protein inhibitor of activated STAT-1 (PIAS1) and the repression of Janus kinase (Jak2) signaling pathways. The data from the present study demonstrated the antitumor effects and the potential pharmacological application of ATR II as an efficient drug for prostate cancer treatment.
AR/PIAS1; ATR II; G2/M arrest; JAK2/STAT3; apoptosis
Atractylenolide II Induces Apoptosis of Prostate Cancer Cells through Regulation of AR and JAK2/STAT3 Signaling Pathways.
Wang J1,2, Nasser MI3, Adlat S4, Ming Jiang M5, Jiang N6, Gao L7.
2018 Dec 12
In the studies of chemoprevention, the Nrf2-ARE signaling pathway has received widespread attention due to its anti-inflammatory and anti-oxidation effects. Our previous study indicated that atractylenolide II, which is an active component of Atractylodes macrocephala Koidz, is a potential activator of Nrf2-ARE signaling pathway. In this study, we observed that atractylenolide II significantly increased Nrf2 expressing, nuclear translocation and the expression of its downstream detoxifying enzymes, thus decreasing 17β-Estradiol induced malignant transformation in MCF 10A cells, and we found that atractylenolide II acted through JNK/ERK-Nrf2-ARE pathway. Furthermore, atractylenolide II significantly reduced N-Nitroso-N-methylurea induced tumor incidence, multiplicity and volume, with activation of Nrf2-ARE pathway and decreased inflammation and oxidative stress in rat mammary tissue. Collectively, our results suggested that atractylenolide II could protect against mammary tumorigenesis both in vivo and in vitro via activating Nrf2-ARE signaling pathway, which supported atractylenolide II as a novel chemopreventive agent of breast cancer.
anti-oxidative response element; atractylenolide II; breast cancer; chemoprevention; nuclear factor (erythroid-derived 2)-like 2
Chemopreventive effects of atractylenolide II on mammary tumorigenesis via activating Nrf2-ARE pathway.
Wang T#1,2, Long F#3, Zhang X1, Yang Y1, Jiang X1, Wang L1.
2017 Aug 24
This investigation was conducted to elucidate whether atractylenolide II could reverse the role of lncRNA XIST/miR-30a-5p/ROR1 axis in modulating chemosensitivity of colorectal cancer cells. We totally collected 294 pairs of colorectal cancer tissues and adjacent normal tissues and also purchased colorectal cancer cell lines and human embryonic kidney cell line. 5-fluorouracil, cisplatin, mitomycin and adriamycin were designated as the chemotherapies for colorectal cell lines, and atractylenolides were arranged as the Chinese drug. The expressions of XIST, miR-30a-5p and ROR1 were quantified with aid of qRT-PCR or Western blot, and luciferase reporter gene assay was implemented to determine the relationships among XIST, miR-30a-5p and ROR1. Our results demonstrated that XIST and ROR1 expressions were dramatically up-regulated, yet miR-30a-5p expression was down-regulated within colorectal cancer tissues (P < 0.05). The overexpressed XIST and ROR1, as well as under-expressed miR-30a-5p, were inclined to promote viability and proliferation of colorectal cells under the influence of chemo drugs (P < 0.05). In addition, XIST could directly target miR-30a-5p, and ROR1 acted as the targeted molecule of miR-30a-5p. Interestingly, atractylenolides not only switched the expressions of XIST, miR-30a-5p and ROR1 within colorectal cancer cells but also significantly intensified the chemosensitivity of colorectal cancer cells (P < 0.05). Finally, atractylenolide II was discovered to slow down the viability and proliferation of colorectal cancer cells (P < 0.05). In conclusion, the XIST/miR-30a-5p/ROR1 axis could be deemed as pivotal markers underlying colorectal cancer, and administration of atractylenolide II might improve the chemotherapeutic efficacy for colorectal cancer.
© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
ROR1; atractylenolide; cell proliferation; cell viability; chemoresistance; colorectal cancer; lncRNA XIST; miR-30a-5p
Atractylenolide II reverses the influence of lncRNA XIST/miR-30a-5p/ROR1 axis on chemo-resistance of colorectal cancer cells.
Zhang R1, Wang Z1, Yu Q2, Shen J1, He W1, Zhou D1, Yu Q1, Fan J1, Gao S1, Duan L3.
Atractylenolide II is a sesquiterpene compound isolated from the dried rhizome of Atractylodes macrocephala (Baizhu in Chinese); anti-proliferative activity.IC50 value: 82.3 μM(B16 melanoma cell, 48 h) Target: anticancer natural compoundin vitro: AT-II treatment for 48 h dose-dependently inhibited cell proliferation with an IC(50) of 82.3 μM, and induced G1 phase cell cycle arrest. Moreover, treatment with 75 μM AT-II induced apoptosis. These observations were associated with the decrease of the expression of Cdk2, phosphorylated-Akt, phosphorylated-ERK and Bcl-2, the increase of the expression of phosphorylated-p38, phosphorylated-p53, p21, p27, and activation of caspases-8, -9 and -3. In addition, a chemical inhibitor of p53, PFTα, significantly decreased AT-II-mediated growth inhibition and apoptosis . In B16 and A375 cells, AT-II (20, 40 μm) treatment for 48 h dose-dependently reduced protein expression levels of phospho-STAT3, phospho-Src, as well as STAT3-regulated Mcl-1 and Bcl-xL. Overexpression of a constitutively active variant of STAT3, STAT3C in A375 cells diminished the antiproliferative and apoptotic effects of AT-II .in vivo: Daily administration of AT-II (12.5, 25 mg/kg, i.g.) for 14 days significantly inhibited tumor growth in a B16 xenograft mouse model and inhibited the activation/phosphorylation of STAT3 and Src in the xenografts .