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Dehydrocostus lactone

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-D1009

  • Specification : 98%

  • CAS number : 477-43-0

  • Formula : C15H18O2

  • Molecular Weight : 230.3

  • PUBCHEM ID : 73174

  • Volume : 20mg

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Catalogue Number

BF-D1009

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

230.3

Appearance

White crystalline powder

Botanical Source

Cyperus rotundus,Aucklandia costus,Dolomiaea souliei,Oxytropis microphylla

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

C=C1CCC2C(C3C1CCC3=C)OC(=O)C2=C

Synonyms

DEHYDROCOSTUNOLIDE/Costus lactone,dehydro/dehydrocustoslactone/(3aS,6aR,9aR,9bS)-3,6,9-trimethylidenedecahydroazuleno[4,5-b]furan-2(3H)-one/(3aS,6aR,9aR,9bS)-3,6,9-Tris(methylene)decahydroazuleno[4,5-b]furan-2(3H)-one/Azuleno[4,5-b]furan-2(3H)-one, decahydro-3,6,9-tris(methylene)-, (3aS,6aR,9aR,9bS)-/EPILIGULYL OXIDE/Dehydrocostus lactone

IUPAC Name

(3aS,6aR,9aR,9bS)-3,6,9-trimethylidene-3a,4,5,6a,7,8,9a,9b-octahydroazuleno[4,5-b]furan-2-one

Density

1.1±0.1 g/cm3

Solubility

Methanol; Acetone; Chloroform; Ethyl Acetate

Flash Point

161.2±25.3 °C

Boiling Point

383.7±42.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C15H18O2/c1-8-4-7-12-10(3)15(16)17-14(12)13-9(2)5-6-11(8)13/h11-14H,1-7H2/t11-,12-,13-,14-/m0/s1

InChl Key

NETSQGRTUNRXEO-XUXIUFHCSA-N

WGK Germany

RID/ADR

HS Code Reference

2932200000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:477-43-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28300289

Abstract

This study evaluates the anticancer effects of dehydrocostus lactone, a plant-derived sesquiterpene lactone, on human chronic myeloid leukemia cells. Dehydrocostus lactone significantly inhibits cell proliferation by inducing cells to undergo cell cycle arrest, apoptosis, and differentiation. Dehydrocostus lactone suppresses the expression of cyclin B1, cyclin A, cyclin E, cyclin-dependent kinase 2 (CDK2), and cyclin-dependent kinase 1 (CDK1) and increases p21 expression, resulting in S-G2/M phase arrest in K562 cells. Dehydrocostus lactone also induces apoptosis by increasing the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (MMP), and modulating the protein levels of Bcl-2 family members. We also found that dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells. At a low concentration, dehydrocostus lactone significantly increased CD11b and CD14 expression on the surface of K562 cells, and induced cells to differentiate into monocytes or mature macrophages. Taken together, this study provides new insight into the molecular mechanisms of dehydrocostus lactone actions that may contribute to the chemoprevention of chronic myeloid leukemia. J. Cell. Biochem. 118: 3381-3390, 2017. © 2017 Wiley Periodicals, Inc.

KEYWORDS

Bcr/Abl; CHRONIC MYELOID LEUKEMIA; DEHYDROCOSTUS LACTONE; STAT PROLIFERATION.

Title

Dehydrocostus Lactone Suppresses Proliferation of Human Chronic Myeloid Leukemia Cells Through Bcr/Abl-JAK/STAT Signaling Pathways

Author

Hong Cai 1 , Xiaosong Qin 2 , Chunhui Yang 1

Publish date

2017 Oct

PMID

10.1002/jcb.25994

Abstract

Dehydrocostus lactone is considered to be the major cholagogic ingredient of the Costus genus of plants. It exhibits strong cholagogic effects, and also exerts antimicrobial and antineoplastic activity. The present study aimed to investigate the effects of dehydrocostus lactone on the cell growth and apoptosis of recombinant human papilloma virus (HPV)‑18 HaCaT cells. The HPV‑18 genome was transfected into HaCaT cells, which were subsequently used for analysis. The results demonstrated that dehydrocostus lactone reduced the cell proliferation and induced apoptosis of HPV‑18 HaCaT cells, as determined by MTT and N‑acetyl‑Asp‑Glu‑Val‑Asp p‑nitroanilide assays, respectively. Furthermore, caspase‑3/9 activity was determined using a caspase‑3/9 activity kit and western blotting was performed to investigate the expression of certain proteins. The results demonstrated that caspase‑3/9 activities, and the protein expression of Bcl‑2‑associated X and p53, in HPV‑18 HaCaT cells were significantly increased, while cyclin D1 protein expression was suppressed by dehydrocostus lactone. Additionally, dehydrocostus lactone significantly upregulated the protein expression of phosphatase and tensin homolog and inhibited the phosphatidylinositol 3‑kinase (PI3K)/Akt signaling pathway in HPV‑18 HaCaT cells. Therefore, the results of the present study indicate that dehydrocostus lactone may suppress cell growth and induce apoptosis in recombinant HPV‑18 HaCaT cells via the PI3K/Akt signaling pathway, and may be a represent a novel potential therapeutic agent for the treatment of condyloma acuminatum.

Title

Induces Apoptosis in Recombinant Human Papilloma virus‑18 HaCaT Cells via the PI3K/Akt Signaling Pathway

Author

Wei Li 1 , Yi Bing Ma 1 , Ying Qiu Mao 2 , Tong Lin 3

Publish date

2018 Jun

PMID

30999647

Abstract

Acute lung injury (ALI) is a severe clinical disease marked by dysregulated inflammation response and has a high rate of morbidity and mortality. Macrophages, which play diverse roles in the inflammatory response, are becoming therapeutic targets in ALI. In this study we investigated the effects of dehydrocostus lactone (DHL), a natural sesquiterpene, on macrophage activation and LPS-induced ALI. The macrophage cell line RAW264.7 and primary lung macrophages were incubated with DHL (0, 3, 5, 10 and 30 μmol/L) for 0.5 h and then challenged with LPS (100 ng/mL) for up to 8 hours. C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) to induce acute lung injury (ALI) and then treated with a range of DHL doses intraperitoneally (5 to 20 mg/kg). The results showed that DHL inhibited LPS-induced production of proinflammatory mediators such as iNOS, NO, and cytokines including TNF-α, IL-6, IL-1β, and IL-12 p35 by suppressing the activity of NF-κB via p38 MAPK/MK2 and Akt signaling pathway in macrophages. The in vivo results revealed that DHL significantly attenuated LPS-induced pathological injury and reduced cytokines expression in the lung. NF-κB, p38 MAPK/MK2 and Akt signaling molecules were also involved in the anti-inflammatory effect. Collectively, our findings suggested that DHL is a promising agent for alleviating LPS-induced ALI.

KEYWORDS

Akt; LPS; NF-κB; acute lung injury; dehydrocostus lactone; macrophage; p38MAPK.

Title

Dehydrocostus Lactone Suppresses LPS-induced Acute Lung Injury and Macrophage Activation Through NF-κB Signaling Pathway Mediated by p38 MAPK and Akt

Author

Yunjuan Nie 1 , Zhongxuan Wang 2 , Gaoshang Chai 3 , Yue Xiong 4 , Boyu Li 5 , Hui Zhang 6 , Ruiting Xin 7 , Xiaohang Qian 8 , Zihan Tang 9 , Jiajun Wu 10 , Peng Zhao 11

Publish date

2019 Apr 17


Description :

Dehydrocostus Lactone is a major sesquiterpene lactone isolated from the roots of Saussurea lappa.IC50 value:Target:In vitro: Dehydrocostus Lactone promoted apoptosis with increased activation of caspases 8, 9, 7, 3, enhanced PARP cleavage, decreased Bcl-xL expression and increased levels of Bax, Bak, Bok, Bik, Bmf, and t-Bid. We have demonstrated that Dehydrocostus Lactone inhibits cell growth and induce apoptosis in DU145 cells [1]. Dehydrocostus Lactone inhibits NF-kappaB activation by preventing TNF-alpha-induced degradation and phosphorylation of its inhibitory protein I-kappaB alpha in human leukemia HL-60 cells and that dehydrocostus lactone renders HL-60 cells susceptible to TNF-alpha-induced apoptosis by enhancing caspase-8 and caspase-3 activities [2]. Dehydrocostus Lactone inhibited the production of NO in lipopolysaccharide (LPS)-activated RAW 264.7 cells by suppressing inducible nitric oxide synthase enzyme expression.In vivo: Dehydrocostus Lactone decreased the TNF-alpha level in LPS-activated systems in vivo [3].