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bavachalcone

$480

  • Brand : BIOFRON

  • Catalogue Number : BD-D0492

  • Specification : HPLC≥98%

  • CAS number : 28448-85-3

  • Formula : C20H20O4

  • Molecular Weight : 324.37

  • PUBCHEM ID : 6450879

  • Volume : 20mg

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Catalogue Number

BD-D0492

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥98%

Storage

2-8°C

Molecular Weight

324.37

Appearance

Yellow crystalline powder

Botanical Source

Psoralea corylifolia L./Broussonetia papyrifera

Structure Type

Chalcones

Category

Standards;Natural Pytochemical;API

SMILES

CC(=CCC1=CC(=C(C=C1O)O)C(=O)C=CC2=CC=C(C=C2)O)C

Synonyms

(2E)-1-[2,4-Dihydroxy-5-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-2-propen-1-one/Bavachalcone/(E)-1-(2,4-Dihydroxy-5-(3-methyl-but-2-enyl)-phenyl)-3-(4-hydroxy-phenyl)-propenone/2-Propen-1-one, 1-[2,4-dihydroxy-5-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-, (2E)-/buroussochalcone B/broussochalcone B

IUPAC Name

(E)-1-[2,4-dihydroxy-5-(3-methylbut-2-enyl)phenyl]-3-(4-hydroxyphenyl)prop-2-en-1-one

Density

1.2±0.1 g/cm3

Solubility

DMSO : ≥ 34 mg/mL (104.82 mM);

Flash Point

300.2±26.6 °C

Boiling Point

549.6±50.0 °C at 760 mmHg

Melting Point

168-169℃

InChl

InChI=1S/C20H20O4/c1-13(2)3-7-15-11-17(20(24)12-19(15)23)18(22)10-6-14-4-8-16(21)9-5-14/h3-6,8-12,21,23-24H,7H2,1-2H3/b10-6+

InChl Key

BLZGPHNVMRXDCB-UXBLZVDNSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:28448-85-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

29156787

Abstract

In cardiovascular diseases, endothelial function is impaired and the level of circulating endothelial progenitor cells (EPCs) is low. This study investigated whether the natural bioactive component bavachalcone (BavaC) induces the differentiation of EPCs and neovascularization in vivo; the underlying mechanisms were also examined. We observed that the treatment of rat bone marrow-derived cells with a very low dose of BavaC significantly promoted EPC differentiation. In our hindlimb ischemia models, low-dose BavaC administered orally for 14 days stimulated the recovery of ischemic hindlimb blood flow, increased circulating EPCs, and promoted capillary angiogenesis. The BavaC treatment of rat bone marrow cells for 24 h initiated the AMP-activated protein kinase (AMPK) activity required for the differentiation of EPCs. Further testing revealed that BavaC and CGP52608, a retinoic acid receptor-related orphan receptor α (RORα) activator, enhanced the activity of RORα1 and EPO luciferase reporter gene. BavaC treatment also elevated EPO mRNA and protein expression in vitro and in vivo and the circulating EPO levels in rats. By contrast, the RORα antagonist VPR66 inhibited BavaC-induced EPO reporter activity, and differentiation of bone marrow cells into endothelial progenitor cells. Overall, this study revealed that BavaC promotes EPC differentiation and neovascularization through a RORα-EPO-AMPK axis. BavaC can be used as a promising angiogenesis agent for enhancing angiogenesis and tissue repair.

KEYWORDS

RORα; bavachlcone; endothelial progenitor cell; erythropoietin; neovascularization.

Title

Natural Compound Bavachalcone Promotes the Differentiation of Endothelial Progenitor Cells and Neovascularization Through the RORα-erythropoietin-AMPK Axis

Author

Shuang Ling 1 , Rong-Zhen Ni 1 2 , Yunyun Yuan 1 , Yan-Qi Dang 1 , Qian-Mei Zhou 1 , Shuang Liang 2 , Fujiang Guo 3 , Wei Feng 4 , Yuanyuan Chen 1 , Katsumi Ikeda 5 , Yukio Yamori 6 , Jin-Wen Xu 1

Publish date

2017 Sep 16

PMID

26199639

Abstract

The circadian clock regulates many aspects of (patho)physiology in the central nervous system and in the peripheral tissues. RAR-related orphan receptor α (RORα), an orphan nuclear receptor, is involved in circadian rhythm regulation, including regulation of cardiovascular function. Bavachalcone, a prenylchalcone, is a major bioactive chalcone isolated from Psoralea corylifolia. This natural ingredient activated RORα1 luciferase reporter activity on drug screening. In addition, bavachalcone induced RORα1 expression in mRNA and protein levels in a dose-dependent manner and enhanced the circadian amplitude of Bmal1 mRNA expression after serum shock. Moreover, bavachalcone suppressed senescence in human endothelial cells and mRNA expression of p16(ink4a) (a marker of replicative senescence) and IL-1α (a proinflammatory cytokine of the senescence-associated secretory phenotype). These inhibitory effects were partially reversed by the RORα inhibitor VPR-66. Our results demonstrate that bavachalcone, as a natural medicine ingredient, has a pharmacological function in regulating RORα1.

KEYWORDS

RORα; bavachlcone; endothelial progenitor cell; erythropoietin; neovascularization.

Title

Bavachalcone Enhances RORα Expression, Controls Bmal1 Circadian Transcription, and Depresses Cellular Senescence in Human Endothelial Cells

Author

Yanqi Dang 1 , Shuang Ling 1 , Jing Ma 1 , Rongzhen Ni 1 , Jin-Wen Xu 1

Publish date

2015

PMID

25766656

Abstract

Mitochondrial oxidative stress has been suggested as a major etiological factor in cardiovascular diseases. Manganese superoxide dismutase (MnSOD) is an essential antioxidant mitochondrial enzyme. Although polyphenols can induce MnSOD expression, their mechanism of action remains unclear. We examined the effect of bavachalcone, a bioactive compound isolated from Psoralea corylifolia, on MnSOD protein expression and explored whether this effect is mediated through the AMP-activated protein kinase (AMPK) signaling pathway. Our data showed that bavachalcone enhanced the luciferase activity of the MnSOD promoter and increased MnSOD mRNA and protein expressions. Moreover, bavachalcone suppressed the mitochondrial superoxide production in endothelial cells. Conversely, bavachalcone stimulated liver kinase B1 and AMPKα phosphorylation. mRNA interference by using short hairpin RNA (shRNA) of AMPK inhibited bavachalcone-induced MnSOD expression. A-769662, an AMPK activator, also stimulated AMPK activity and increased MnSOD expression. Furthermore, AMPK knockdown by shRNA-AMPK reversed the inhibitory effects of bavachalcone on mitochondrial superoxide production in endothelial cells. These findings indicate that bavachalcone can protect the endothelial function by increasing AMPK activity and MnSOD expression and reducing mitochondrial oxidative stress. .

Title

Bavachalcone-induced Manganese Superoxide Dismutase Expression Through the AMP-activated Protein Kinase Pathway in Human Endothelial Cells

Author

Yanqi Dang 1 , Shuang Ling, Ju Duan, Jing Ma, Rongzhen Ni, Jin-Wen Xu

Publish date

2015


Description :

Bavachalcone is a major bioactive compounds isolated from Psoralea corylifolia L.; has been widely used as traditional Chinese medicine; antibiotic or anticancer agent.IC50 value:Target:Bavachalcone inhibited osteoclast formation from precursor cells with the IC(50) of approximately 1.5 microg ml(-1). The activation of MEK, ERK, and Akt by receptor activator of nuclear factor kappaB ligand (RANKL), the osteoclast differentiation factor, was prominently reduced in the presence of bavachalcone. The induction of c-Fos and NFATc1, key transcription factors for osteoclastogenesis, by RANKL was also suppressed by bavachalcone [1]. Bavachalcone exhibited a significant inhibitory effect on baculovirus-expressed BACE-1 in vitro [2]. Bavachalcone had stronger inhibition on UGT1A1 and UGT1A7 than corylin which did not inhibit UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A10, and UGT2B4. Data fitting using Dixon and Lineweaver-Burk plots demonstrated the noncompetitive inhibition of bavachalcone against UGT1A1 and UGT1A7-mediated 4-MU glucuronidation reaction. The values of inhibition kinetic parameters (Ki) were 5.41 μ M and 4.51μ M for UGT1A1 and UGT1A7, respectively [3].