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Loureirin B

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-L3014

  • Specification : 98%

  • CAS number : 119425-90-0

  • Formula : C18H20O5

  • Molecular Weight : 316.35

  • PUBCHEM ID : 189670

  • Volume : 25mg

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Catalogue Number

BF-L3014

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

316.35

Appearance

White powder

Botanical Source

Dracaena cochinchinensis

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC(=C(C(=C1)OC)CCC(=O)C2=CC=C(C=C2)O)OC

Synonyms

1-Propanone,1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)/1-Propanone, 1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)-/Loureirin B/LR-B/1-(4-Hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)-1-propanone/1-(4-Hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)propan-1-one

IUPAC Name

1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)propan-1-one

Density

1.2±0.1 g/cm3

Solubility

Methanol; Dichloromethane

Flash Point

184.0±23.6 °C

Boiling Point

509.9±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C18H20O5/c1-21-14-10-17(22-2)15(18(11-14)23-3)8-9-16(20)12-4-6-13(19)7-5-12/h4-7,10-11,19H,8-9H2,1-3H3

InChl Key

ZPFRAPVRYLGYEC-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#:119425-90-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28817206

Abstract

The development of new diabetes drugs continues to be explored. Loureirin B, a flavonoid, extracted from Dracaena cochinchinensis, has been confirmed to increase insulin secretion and decrease blood glucose levels. For searching the promotion of insulin secretion with the treatment of loureirin B, experiments were employed based on cell experiments and computational methods. First, promotion of insulin secretion was dependent on extracellular glucose concentration. At the genetic level, loureirin B enhanced the relative mRNA level of Pdx-1 and MafA. Meanwhile the intracellular level of ATP increased due to the continuous absorption of glucose. Further experiments showed that the currents of KATP channel on Ins-1 cells were inhibited and the voltage-dependent calcium channels were subsequently activated. The increase of Cx43 protein expression might mediate the Ca2+ to the intracellular. Through computational simulation, we hypothesized that loureirin B might interact with KATP channels to promote insulin secretion. In conclusion, it could be concluded that loureirin B promoted insulin secretion mainly through increasing mRNA level of Pdx-1, MafA, intracellular ATP level, inhibiting the KATP current, influx of Ca2+ to the intracellular.

KEYWORDS

KATP channel; influx of Ca; ins-1 cells; insulin secretion; loureirin B.

Title

Loureirin B Promotes Insulin Secretion Through Inhibition of K ATP Channel and Influx of Intracellular Calcium

Author

Yijie Sha 1 , Yuelin Zhang 1 , Jing Cao 2 , Kai Qian 2 , Bing Niu 1 , Qin Chen 1

Publish date

2018 Feb

PMID

30123297

Abstract

Background: We investigated the activity of loureirin B against liver fibrosis and the underlying molecular mechanisms.
Methods: Hepatic stellate cells (HSCs) from Sprague-Dawley rats were treated with different concentrations of loureirin B. We used the MTT assay to determine HSC proliferation, flow cytometry to analyze apoptosis, and western blot to determine the expressions of Bax, Bcl-2, Wnt1 and β-catenin. Real-time PCR was used to determine the expressions of Wnt1 and miR-148-3p.
Results: The MTT assay showed that loureirin B treatment significantly inhibited the proliferation of HSCs in time- and dose-dependent manners. Loureirin B significantly promoted the apoptosis of HSCs, increased the expression of Bax and decreased the Bcl-2 level. Western blot analysis showed that the expressions of Wnt1 and β-catenin were obviously lower in the loureirin B treatment group than in the control group. We also found that loureirin B could decrease the Wnt1 mRNA level and increase miR-148-3p expression. Knockdown of miR-148-3p using inhibitor could reverse the effects of loureirin B on the proliferation and apoptosis of HSCs and the expressions of Bax, Bcl-2, Wnt1 and β-catenin.
Conclusion: Our results suggest that loureirin B inhibited the proliferation and promoted the apoptosis of HSCs, and suppressed the Wnt/β-catenin signaling pathway via regulation of miR-148-3p.

KEYWORDS

Hepatic stellate cells; Liver fibrosis; Loureirin B; Wnt1; miR-148-3p.

Title

Loureirin B Inhibits the Proliferation of Hepatic Stellate Cells and the Wnt/β-catenin Signaling Pathway by Regulating miR-148-3p

Author

Jian-Peng Hu # 1 , Rong Zhang # 1 , Min Tang 2 , Yu-Lian Li 2 , Lin-Ting Xun 2 , Zhi-Zhou Shi 1 , Ying An 2 , Ting Li 2 , Zheng-Ji Song 2

Publish date

. 2018 Aug 2

PMID

25683490

Abstract

The ethanolic extract of Resina Draconis (RDEE) has been reported beneficial to normal wound healing yielding more regularly arranged collagen fibres. Loureirin B, a major component in RDEE, has been supposed to be effective on the prevention and treatment of pathological scars. To investigate the therapeutic effects of loureirin B on hypertrophic scar (HS), fibroblasts from human HS and normal skin (NS) were isolated. Results showed that loureirin B dose-dependently downregulated both mRNA and protein levels of type I collagen (ColI), type III collagen (ColIII) and α-smooth muscle actin (α-SMA) in HS fibroblasts. Loureirin B also suppressed fibroblast proliferative activity and redistributed cell cycle, but did not affect cell apoptosis. In vivo rabbit ear scar model, loureirin B significantly improved the arrangement and deposition of collagen fibres, decreased protein levels of ColI, ColIII and α-SMA and suppressed myofibroblast differentiation and scar proliferative activity. In NS fibroblasts, loureirin B effectively inhibited TGF-β1-induced upregulation of ColI, ColIII and α-SMA levels, myofibroblast differentiation and the activation of Smad2 and Smad3. Loureirin B also affected mRNA levels of major MMPs and TIMPs in TGF-β1-stimulated fibroblasts. Taken together, this study demonstrates that loureirin B could downregulate the expression of fibrosis-related molecules by regulating MMPs and TIMPs levels, inhibit scar fibroblast proliferation and suppress TGF-β1-induced fibrosis, during which TGF-β1/Smad2/3 pathway is likely involved. These findings suggest that loureirin B is a potential therapeutic compound for HS treatment.

KEYWORDS

TGF-β/Smad; extracellular matrix; fibroblasts; hypertrophic scar; loureirin B.

Title

Loureirin B Inhibits Fibroblast Proliferation and Extracellular Matrix Deposition in Hypertrophic Scar via TGF-β/Smad Pathway

Author

Xiaozhi Bai 1 , Ting He, Jiaqi Liu, Yunchuan Wang, Lei Fan, Ke Tao, Jihong Shi, Chaowu Tang, Linlin Su, Dahai Hu

Publish date

2015 May


Description :

Loureirin B, a flavonoid extracted from Dracaena cochinchinensis, is an inhibitor of plasminogen activator inhibitor-1 (PAI-1), with an IC50 of 26.10 μM; Loureirin B also inhibits KATP, the phosphorylation of ERK and JNK, and has anti-diabetic activity.