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Levistolide A

$143

  • Brand : BIOFRON

  • Catalogue Number : BF-L2023

  • Specification : 98%

  • CAS number : 88182-33-6

  • Formula : C24H28O4

  • Molecular Weight : 380

  • PUBCHEM ID : 70698035

  • Volume : 20mg

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Catalogue Number

BF-L2023

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

380

Appearance

White crystalline

Botanical Source

Ligusticum sinense cv. chuanxiong,Angelica sinensis,Ligusticum sinense,Heracleum hemsleyanum

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CCCC=C1C2=C(C3C(CC2)C4CCC35C(=C4)C(=O)OC5=CCCC)C(=O)O1

Synonyms

(1S,2S,6Z,10S,11S,16Z)-6,16-Dibutylidene-5,15-dioxapentacyclo[9.5.2.0.0.0]octadeca-3(7),12-diene-4,14-dione/diligustilide/1H-5,10c-Ethanonaphtho[1,2-c:7,8-c']difuran-3,10-dione, 1,8-dibutylidene-5,5a,6,7,8,10b-hexahydro-, (1Z,5S,5aS,8Z,10bS,10cS)-

IUPAC Name

(1S,2S,6Z,10S,11S,16Z)-6,16-di(butylidene)-5,15-dioxapentacyclo[9.5.2.01,13.02,10.03,7]octadeca-3(7),12-diene-4,14-dione

Density

1.2±0.1 g/cm3

Solubility

Methanol; Ethanol

Flash Point

325.7±29.9 °C

Boiling Point

623.8±55.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C24H28O4/c1-3-5-7-18-16-10-9-15-14-11-12-24(21(15)20(16)23(26)27-18)17(13-14)22(25)28-19(24)8-6-4-2/h7-8,13-15,21H,3-6,9-12H2,1-2H3/b18-7-,19-8-/t14-,15+,21-,24+/m1/s1

InChl Key

UBBRXVRQZJSDAK-ZJHGLIIDSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:88182-33-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28662507

Abstract

BACKGROUND/AIMS:
Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Levistolide A (LA), a natural compound isolated from the traditional Chinese herb Ligusticum chuanxiong Hort, is used for treating cancer. In this study, we investigated the anticancer effect of LA in HCT116 and its isogenic p53-/- colon cancer cells, as well as the underlying mechanisms.

METHODS:
MTT assay was used to evaluate the effect of LA on the viability of cancer cells. Apoptosis and reactive oxygen species (ROS) production by the cells were determined by flow cytometry. Protein expression was detected by western blotting.

RESULTS:
The results showed that LA inhibited viability and caused apoptosis of both wild-type and p53-/- HCT116 cells. LA was able to trigger production of ROS and endoplasmic reticulum (ER) stress. Inhibition of ROS using N-acetylcysteine abrogated LA-induced ER stress and apoptosis, as well as the reduction in cancer cell viability.

CONCLUSION:
Our results indicate that LA causes apoptosis of colon cancer cells via ROS-mediated ER stress pathway. It will be interesting to develop the natural compound for chemotherapy of cancers such as CRC.

© 2017 The Author(s). Published by S. Karger AG, Basel.

KEYWORDS

Apoptosis; ER stress; Levistolide A; ROS

Title

Levistolide A Induces Apoptosis via ROS-Mediated ER Stress Pathway in Colon Cancer Cells.

Author

Yang Y, Zhang Y, Wang L, Lee S.

Publish date

2017

PMID

30483812

Abstract

Multidrug resistance (MDR) is one of the main reasons underlying failure of cancer chemotherapy. Certain natural compounds may help prevent MDR, and may be used in combination with chemotherapeutic agents to enhance their efficacy. Levistolide A is a natural product that is extracted from the rhizome of Angelicae sinensis (Oliv.), which has been used as an essential component of antitumor formulas since ancient times in China. The present study conducted the following experiments: MTT assay, apoptosis analysis, cellular doxorubicin accumulation assay, immunoblotting and reverse transcription‑quantitative polymerase chain reaction, to investigate whether levistolide A enhance doxorubicin‑induced apoptosis of k562/dox cells and to determine the molecular mechanisms involved. When combined with doxorubicin, levistolide A exhibited a synergistic effect and induced cytotoxicity in k562/dox cells. Drug accumulation studies revealed that levistolide A increased the intracellular concentration of doxorubicin in a dose‑dependent manner. Cell apoptosis experiments indicated that levistolide A increased the sensitivity of k562/dox cells to doxorubicin. Furthermore, detection of reactive oxygen species (ROS) revealed that levistolide A enhanced doxorubicin‑induced cell death by increasing the levels of ROS. Mitochondrial potential detection with JC‑1 staining also indicated that levistolide A synergistically enhanced doxorubicin‑induced cell death. Immunoblotting demonstrated that levistolide A enhanced doxorubicin‑induced cell death by decreasing the expression levels of B‑cell lymphoma 2 and increasing caspase 3 expression. Furthermore, multidrug resistance protein 1 (MDR1) expression in k562/dox cells was downregulated by levistolide A in a dose‑dependent manner, thus suggesting that levistolide A may modulate MDR1 during cancer therapy. Therefore, the combination of levistolide A with doxorubicin could result in more effective and less toxic anticancer regimens.

Title

Levistolide A synergistically enhances doxorubicin‑induced apoptosis of k562/dox cells by decreasing MDR1 expression through the ubiquitin pathway.

Author

Ding Y1, Niu W2, Zhang T3, Wang J3, Cao J3, Chen H1, Wang R1, An H1.

Publish date

2019 Feb

PMID

18358092

Abstract

AIM:
The aim of the present study was to investigate the reversing effect of levistolide A (LA) on P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) in human breast carcinoma Bcap37/MDR1 cells.

METHODS:
After chemotherapeutic drugs (adriamycin or vincristine) used alone or in combination with LA, cell proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay and cell cycle distribution by flow cytometry. RT-PCR was used to detect MDR1 gene transcription and the Western blot assay was used to assess P-gp expression and the cleavages of poly(ADP-ribose) polymerase and caspase-3. Apoptosis was detected by terminal transferase-mediated dUTP nick end-labeling assay. Moreover, the P-gp function was evaluated by the intracellular accumulation of the P-gp substrate detected by flow cytometry.

RESULTS:
We found the subcytotoxic doses of LA significantly enhanced adriamycin- or vincristine- induced G2/M arrest and apoptosis. These effects were consistent with the ability of LA to inhibit P-gp function. Moreover, LA dramatically enhanced the verapamil (VER) ability to reverse drug resistance.

CONCLUSION:
LA has the potential to be developed as a novel P-gp modulator. Furthermore, the combination of LA and VER might represent a more sufficient but less toxic anti-MDR regimen.

Title

Levistolide A overcomes P-glycoprotein-mediated drug resistance in human breast carcinoma cells.

Author

Chen F1, Wang T, Wang J, Wang ZQ, Qian M.

Publish date

2008 Apr


Description :

Levistolide A overcomes P-glycoprotein-mediated drug resistance in human breast carcinoma cells. PUMID/DOI:18358092 Acta Pharmacol Sin. 2008 Apr;29(4):458-64. The aim of the present study was to investigate the reversing effect of levistolide A (LA) on P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) in human breast carcinoma Bcap37/MDR1 cells.||METHODS:||After chemotherapeutic drugs (adriamycin or vincristine) used alone or in combination with LA, cell proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay and cell cycle distribution by flow cytometry. RT-PCR was used to detect MDR1 gene transcription and the Western blot assay was used to assess P-gp expression and the cleavages of poly(ADP-ribose) polymerase and caspase-3. Apoptosis was detected by terminal transferase-mediated dUTP nick end-labeling assay. Moreover, the P-gp function was evaluated by the intracellular accumulation of the P-gp substrate detected by flow cytometry.||RESULTS:||We found the subcytotoxic doses of LA significantly enhanced adriamycin- or vincristine- induced G2/M arrest and apoptosis. These effects were consistent with the ability of LA to inhibit P-gp function. Moreover, LA dramatically enhanced the verapamil (VER) ability to reverse drug resistance.||CONCLUSION:||LA has the potential to be developed as a novel P-gp modulator. Furthermore, the combination of LA and VER might represent a more sufficient but less toxic anti-MDR regimen.