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Hyperoside

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-H1007

  • Specification : 98%

  • CAS number : 482-36-0

  • Formula : C21H20O12

  • Molecular Weight : 464.38

  • PUBCHEM ID : 5281643

  • Volume : 20mg

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Catalogue Number

BF-H1007

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

464.38

Appearance

Yellow crystalline powder

Botanical Source

Leonurus japonicus,Blumea balsamifera,Prunella vulgaris,Rhododendron dauricum,Melia azedarach

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1C2=C(C(=O)C3=C(C=C(C=C3O2)O)O)OC4C(C(C(C(O4)CO)O)O)O)O)O

Synonyms

2-(3,4-Dihydroxyphenyl)-3-(β-D-galactopyranosyloxy)-5,7-dihydroxy-4H-1-benzopyran-4-one/Quercetin 3-O-β-D-galactoside/quercetin-3-O-galactoside/Hyperin/Quercetin 3-O-galactoside/Quercetin 3-β-D-galactopyranoside/Hyperoside/Quercetin 3-O-β-D-galactopyranoside/Quercetin-3-O-β-D-galactoside/Hyperasid/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-3-(β-D-galactopyranosyloxy)-5,7-dihydroxy-/Hyperosid/quercetin-3-β-O-galactoside/Quercetin 3-galactoside/quercetin 3-O-beta-D-galactopyranoside/2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-4-oxo-4H-chromen-3-yl β-D-galactopyranoside/hyperozide/Quercetin 3-D-galactoside/quercetin-3-galactoside

IUPAC Name

2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one

Density

1.9±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

307.5±27.8 °C

Boiling Point

872.6±65.0 °C at 760 mmHg

Melting Point

225-226ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:482-36-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30257331

Abstract

Hyperoside, an active flavonoid glycoside isolated from many traditional Chinese medicines, has received much attention because of its potential role in osteoporosis treatment. In the present study, we investigated the antiosteoporotic role and mechanism of hyperoside on ovariectomized (OVX) mice. Sixty female Kunming mice received one of three treatments orally for 12 weeks: estradiol valerate (0.3 mg/kg body weight/day), hyperoside (20, 40, or 80 mg/kg body weight/day), or vehicle. We found that hyperoside was effective in preventing osteoporosis by increasing bone mineral density, restoring trabecular bone micro-architecture, and enhancing bone strength. Meanwhile, the activities of bone resorption markers, including tartrate-resistant acid phosphatase 5b (TRAP-5b) and C-terminal telopeptide of type I collagen (CTX), were significantly decreased, while the bioactivity of bone formation markers, osteocalcin (OC) and bone-specific alkaline phosphatase (BALP), were significantly increased. Mechanistically, hyperoside reduced the expression of receptor activator of nuclear factor-κB ligand (RANKL), TNF-receptor-associated factor 6 (TRAF6), phosphorylated inhibitor of nuclear factor-κB α (IκBα), NF-kB p65, and nuclear factor of activated T cell cytoplasmic 1 (NFATc1) and promoted the expression of osteoprotegerin (OPG). Therefore, the function of hyperoside might be related to the inhibition of the TRAF-6 mediated RANKL/RANK/NF-κB signaling pathway and the elevation of the OPG/RANKL ratio. These data demonstrated that hyperoside has potential applications as a drug for osteoporosis treatment.
Copyright © 2018. Published by Elsevier Masson SAS.

KEYWORDS

Hyperoside; NFATc1; OPG/RANKL; Osteoporosis; Ovariectomy; TRAF6

Title

Beneficial effects of hyperoside on bone metabolism in ovariectomized mice.

Author

Chen Y1, Dai F2, He Y3, Chen Q4, Xia Q5, Cheng G6, Lu Y7, Zhang Q8.

Publish date

2018 Nov

PMID

28810631

Abstract

Pseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infection and is readily able to form biofilms. Due to its high antibiotic resistance, traditional antibacterial treatments exert a limited effect on P. aeruginosa biofilm infections. It has been indicated that hyperoside inhibits P. aeruginosa PAO1 (PAO1) biofilm formation without affecting growth. Therefore, the current study examined the biofilm formation and quorum sensing (QS) system of PAO1 in the presence of hyperoside. Confocal laser scanning microscopy analysis demonstrated that hyperoside significantly inhibited biofilm formation. It was also observed that hyperoside inhibited twitching motility in addition to adhesion. Data from reverse transcription-quantitative polymerase chain reaction indicated that hyperoside inhibited the expression of lasR, lasI, rhlR and rhlI genes. These results suggest that the QS-inhibiting effect of hyperoside may lead to a reduction in biofilm formation. However, the precise mechanism of hyperoside on P. aeruginosa pathogenicity remains unclear and requires elucidation in additional studies.

KEYWORDS

Pseudomonas aeruginosa; adhesion; biofilm; hyperoside; quorum sensing; twitching motility

Title

Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa.

Author

Sun Y1, Sun F1, Feng W1, Qiu X1, Liu Y1, Yang B1, Chen Y1, Xia P1.

Publish date

2017 Aug

PMID

31353051

Abstract

Heart failure (HF) is an end-stage of various serious cardiovascular diseases, which causes liver injury. Hyperoside has been reported to exert protective effect on liver injury and fibrosis. However, the role and related mechanisms of hyperoside in HF-induced liver fibrosis are still unclear. In the current study, we established a model of HF via aortocaval fistula (ACF) in rats in vivo. Hyperoside treatment in ACF rats increased cardiac output, the maximum peak rate of rise/fall in left ventricular pressure (+dP/dt, -dP/dt) and LV ejection fraction (LVEF), decreased LV end-systolic pressure (LVESP), LV end-diastolic pressure (LVEDP) and LV end-systolic volume (LVESV), and reduced heart weight/body weight ratio in a dose-dependent manner. Moreover, hyperoside could attenuate liver fibrosis and injury in ACF rats, as evidenced by reduction of fibrosis area and hydroxyproline content, amelioration of edema and degeneration of liver cell vacuoles, and inhibition of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels. Further, α-smooth-muscle actin (α-SMA), collagen I, profibrotic factor-connective tissue growth factor (CTGF), matrix metalloproteinase-2 (MMP2) and MMP9 levels were down-regulated in hyperoside-treated ACF rats. Additionally, hyperoside inhibited the activation of TGF-β1/Smad pathway. Finally, we confirmed that hyperoside suppressed TGF-β1-mediated hepatic stellate cell activation in vitro. Collectively, hyperoside showed a suppressive role in HF-induced liver fibrosis and injury.
Copyright © 2019 Elsevier GmbH. All rights reserved.

KEYWORDS

Fibrosis; Heart failure; Hyperoside; Liver injury

Title

Hyperoside protects against heart failure-induced liver fibrosis in rats.

Author

Guo X1, Zhu C2, Liu X1, Ge Y1, Jiang X1, Zhao W3.

Publish date

2019 Oct


Description :

Hyperoside, a natural flavonoid, isolated from Camptotheca acuminate, possesses antifungal, anti-inflammatory, anti-viral, anti-oxidative and anti-apoptotic activities[1].