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Oroxylin A

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-O2004

  • Specification : 98%

  • CAS number : 480-11-5

  • Formula : C16H12O5

  • Molecular Weight : 284.26

  • PUBCHEM ID : 5320315

  • Volume : 20mg

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Catalogue Number

BF-O2004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

284.26

Appearance

Yellow needle crystal

Botanical Source

seeds of Oraxylum indicum (L.) Kurz

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C2=C(C=C1O)OC(=CC2=O)C3=CC=CC=C3)O

Synonyms

Oroxylin/4H-1-Benzopyran-4-one, 5,7-dihydroxy-6-methoxy-2-phenyl-/baicalein 6-methyl ether/5,7-Dihydroxy-6-methoxy-2-phenyl-4H-chromen-4-one/5,7-Dihydroxy-6-methoxyflavone/6-Methoxybaicalein/oroxyllin-A/6-methoxy-5,7-dihydroxyflavone/5,7-Dihydroxy-6-methoxy-2-phenyl-4H-1-benzopyran-4-one/oroxylin A/5,7-Dihydroxy-6-methoxy-2-phenyl-4H-1-benzopyran-4-one 5,7-Dihydroxy-6-methoxyflavone/5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one/4H-1-Benzopyran-4-one,5,7-dihydroxy-6-methoxy-2-phenyl

IUPAC Name

5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one

Density

1.4±0.1 g/cm3

Solubility

Methanol

Flash Point

207.4±23.6 °C

Boiling Point

540.9±50.0 °C at 760 mmHg

Melting Point

195-197ºC

InChl

InChI=1S/C16H12O5/c1-20-16-11(18)8-13-14(15(16)19)10(17)7-12(21-13)9-5-3-2-4-6-9/h2-8,18-19H,1H3

InChl Key

LKOJGSWUMISDOF-UHFFFAOYSA-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#:480-11-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31610205

Abstract

Proliferation and differentiation of hepatic stellate cells (HSCs) are the most noticeable events in hepatic fibrosis, in which the loss of lipid droplets (LDs) is the most important feature. However, the complex mechanisms of LD disappearance have not been fully elucidated. In the current study, we investigated whether oroxylin A has the pharmacological activity of reversing LDs in activated HSCs, and further examined its potential molecular mechanisms. Using genetic, pharmacological, and molecular biological measure, we found that LD content significantly decreased during HSC activation, whereas oroxylin A markedly reversed LD content in activated HSCs. Interestingly, oroxylin A treatment observably decreased the expression of adipose triglyceride lipase (ATGL) without large differences in classical LD synthesis pathway, LD-related transcription factors, and autophagy pathway. ATGL overexpression could completely impair the effect of oroxylin A on reversing LD content. Importantly, reactive oxygen species (ROS) signaling pathway mediated oroxylin A-induced ATGL downregulation and LD revision in activated HSCs. ROS specific stimulant buthionine sulfoximine (BSO) could dramatically diminish the antioxidant effect of oroxylin A, and in turn, abolish reversal effect of oroxylin A on LD content. Conversely, ROS specific scavenger N-acetyl cystenine (NAC) can significantly enhance the pharmacological effect of oroxylin A on LD revision. Taken together, our study reveals the important molecular mechanism of anti-fibrosis effect of oroxylin A, and also suggests that ROS-ATGL pathway is a potential target for reversing LDs.

Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS

ATGL; Hepatic stellate cell; Lipid droplet; Oroxylin A; ROS

Title

Oroxylin A regulates the turnover of lipid droplet via downregulating adipose triglyceride lipase (ATGL) in hepatic stellate cells.

Author

Zhang Z1, Guo M2, Shen M1, Li Y1, Tan S3, Shao J4, Zhang F1, Chen A5, Wang S6, Zheng S7.

Publish date

2019 Dec 1;

PMID

31341911

Abstract

Oroxylin A is a natural extract and has been reported to have a remarkable anticancer function. However, the mechanism of its anticancer activity remains not quite clear. In this study, we examined the inhibiting effects of Oroxylin A on breast cancer cell proliferation, migration, and epithelial-mesenchymal transition (EMT) and its possible molecular mechanism. The cytoactive and inflammatory factors were analyzed via Cell Counting Kit-8 assay and ELISA assay, respectively. Flow cytometry and western blotting were used to assess the cell proliferation. In addition, a wound healing assay and transwell assay were used to detect cell invasion and migration. qRT-PCR and western blot were employed to determine the effect of Oroxylin A on the EMT formation. Moreover, expression level of protein related to NF-κB signaling pathway was determined by western blot. The results revealed that Oroxylin A attenuated the cytoactivity of MDA-MB-231 cells in a dose- and a time-dependent manner. Moreover, cell proliferation, invasion, and migration of breast cancer cells were inhibited by Oroxylin A compared to the control. The mRNA and protein expression levels of E-cadherin were remarkably increased while N-cadherin and Vimentin remarkably decreased. Besides, Oroxylin A suppressed the expression of inflammatory factors and NF-κB activation. Furthermore, we also found that supplement of TNF-α reversed the effects of Oroxylin A on the cell proliferation, invasion, migration, and EMT in breast cancer cells. Taken together, our results suggested that Oroxylin A inhibited the cell proliferation, invasion, migration, and EMT through inactivating NF-κB signaling pathway in human breast cancer cells. These findings strongly suggest that Oroxylin A could be a therapeutic potential candidate for the treatment of breast cancer.

Title

Oroxylin A Suppresses the Cell Proliferation, Migration, and EMT via NF-κB Signaling Pathway in Human Breast Cancer Cells.

Author

Sun X1,2,3, Chang X1,2,3, Wang Y4, Xu B4, Cao X1,2,3.

Publish date

2019 Jun 23

PMID

30744936

Abstract

Studies on the efficacy evaluation of UDP-glucuronosyltransferases (UGTs) substrates often ignore the existence of active metabolites. However, the present study aims to establish an in-vitro Phase II metabolism system to predict their pharmacological effects after metabolism. Rat liver microsomes (RLMs) encapsulated in a F127′-Acr-Bis (FAB) hydrogel were placed in the incubation system. Baicalein (BA) was chosen as a model drug and the metabolic activity was investigated by quantitating the metabolite Baicalin (BG). The 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay was used to measure the cell viability in Traditional cell culture system (TCCS) and Microsome-hydrogel added to cell culture system for Phase II metabolism (MHCCS-II). Finally, MHCCS-II was applied to predict the metabolic effects of Oroxylin A (OA) and Wogonin (W). Compared to TCCS group, for HepG2 and MCF-7 cells, BA in MHCCS-II led to lower survival ratios of cells (P < 0.05), while for PC12 cells it led to higher survival ratios of cells (P < 0.01). For HepG2 cells, OA and W showed obviously enhanced tumor inhibition after metabolism with the IC50 of 32.7 ± 2.9 μM and 76.1 ± 5.1 μM, respectively (P < 0.01). In conclusion, the MHCCS-II could be a useful tool for studying the pharmacokinetics and pharmacodynamics of UGTs substrates.

Copyright © 2019 The Japanese Society for the Study of Xenobiotics. Published by Elsevier Ltd. All rights reserved.

KEYWORDS

Baicalein; FAB hydrogel; Liver microsome; Phase II metabolism; UGT

Title

Establishment of rat liver microsome-hydrogel system for in vitro phase II metabolism and its application to study pharmacological effects of UGT substrates.

Author

Zhang Z1, Ma G1, Xue C1, Sun H1, Wang Z1, Xiang X2, Cai W3

Publish date

2019 Apr


Description :

Oroxylin A is a natural active flavonoid with strong anticancer effects.IC50 value:Target:In vitro: Oroxylin A suppressed the MDM2-mediated degradation of p53 via downregulating MDM2 transcription in wt-p53 cancer cells [1]. Oroxylin A remarkably reduced the generation of lactate and glucose uptake under hypoxia in HepG2 cells, inhibited HIF-1α expression and its stability [2]. Oroxylin A promotes superoxide dismutase (SOD2) gene expression through SIRT3-regulated DNA-binding activity of FOXO3a and increases the activity of SOD2 by promoting SIRT3-mediated deacetylation [3]. In vivo: Oroxylin A inhibited the tumor growth of nude mice-inoculated MCF-7 or HCT116 cells. The expression of MDM2 protein in tumor tissue was downregulated by oroxylin A as well [1]