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Hydrangenol

$780

  • Brand : BIOFRON

  • Catalogue Number : AV-C10465

  • Specification : 98%

  • CAS number : 480-47-7

  • Formula : C15H12O4

  • Molecular Weight : 256.3

  • PUBCHEM ID : 119199

  • Volume : 5mg

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Catalogue Number

AV-C10465

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

256.3

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1C(OC(=O)C2=C1C=CC=C2O)C3=CC=C(C=C3)O

Synonyms

3,4-Dihydro-8-hydroxy-3-(4-hydroxyphenyl)-1H-2-benzopyran-1-one/Hydrangenol/8-Hydroxy-3-(4-hydroxyphenyl)-3,4-dihydro-1H-isochromen-1-one/8-hydroxy-3-(4-hydroxyphenyl)-3,4-dihydroisochromen-1-one/1H-2-Benzopyran-1-one, 3,4-dihydro-8-hydroxy-3-(4-hydroxyphenyl)-/8-Hydroxy-3-(4-hydroxy-phenyl)-isochroman-1-one

IUPAC Name

8-hydroxy-3-(4-hydroxyphenyl)-3,4-dihydroisochromen-1-one

Applications

Density

1.4±0.1 g/cm3

Solubility

AP-1; MAPK; MMPs; collagen; hydrangenol; photoaging; skin moisture; ultraviolet B; wrinkle formation

Flash Point

206.4±23.6 °C

Boiling Point

528.3±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C15H12O4/c16-11-6-4-9(5-7-11)13-8-10-2-1-3-12(17)14(10)15(18)19-13/h1-7,13,16-17H,8H2

InChl Key

DGKDFNDHPXVXHW-UHFFFAOYSA-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#:480-47-7) 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

31581754

Abstract

Our previous study showed that hydrangenol isolated from Hydrangea serrata leaves exerts antiphotoaging activity in vitro. In this study, we determined its antiphotoaging effect in UVB-irradiated HR-1 hairless mice. We evaluated wrinkle formation, skin thickness, histological characteristics, and mRNA and protein expression using qRT-PCR and Western blot analysis in dorsal skins. Hydrangenol mitigated wrinkle formation, dorsal thickness, dehydration, and collagen degradation. Hydrangenol increased the expression of involucrin, filaggrin, and aquaporin-3 (AQP3) as well as hyaluronic acid (HA) production via hyaluronidase (HYAL)-1/-2 downregulation. Consistent with the recovery of collagen composition, the expression of Pro-COL1A1 was increased by hydrangenol. Matrix metalloproteinase (MMP)-1/-3, cyclooxygenase-2 (COX-2), and interleukin-6 (IL-6) expression was reduced by hydrangenol. Hydrangenol attenuated the phosphorylation of mitogen-activated protein kinases (MAPKs) including ERK and p38, activator protein 1 (AP-1) subunit, and signal transduction and activation of transcription 1 (STAT1). Hydrangenol upregulated the expression of nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO-1), glutamate cysteine ligase modifier subunit (GCLM), and glutamate cysteine ligase catalysis subunit (GCLC). Taken together, our data suggest that hydrangenol can prevent wrinkle formation by reducing MMP and inflammatory cytokine levels and increasing the expression of moisturizing factors and antioxidant genes.

KEYWORDS

AP-1; MAPK; MMPs; collagen; hydrangenol; photoaging; skin moisture; ultraviolet B; wrinkle formation

Title

Hydrangenol Isolated from the Leaves of Hydrangea serrata Attenuates Wrinkle Formation and Repairs Skin Moisture in UVB-Irradiated Hairless Mice.

Author

Myung DB1,2, Han HS3,4, Shin JS5, Park JY6,7, Hwang HJ8,9, Kim HJ10, Ahn HS11, Lee SH12, Lee KT13,14.

Publish date

2019 Oct 2

PMID

30034317

Abstract

Hydrangenol is a dihydroisocoumarin that is mainly obtained from Hydrangea macrophylla. Recently, hydrangenol has garnered attention since several studies have reported that it has anti-inflammatory, anti-allergic, anti-diabetic, and anti-malarial activities. However, there have been few studies on the effect of hydrangenol on oncogenesis. In this study, we evaluated the anti-cancer activity of hydrangenol against the EJ bladder cancer cell line. Hydrangenol significantly inhibited the proliferation of EJ cells in a dose-dependent manner with an IC50 of 100 ?M. Flow cytometry and immunoblotting experiments indicated that EJ cells were arrested in the G1-phase of the cell cycle and showed reduced expression of CDK2, CDK4, cyclin D1, and cyclin E mediated via the upregulation of p21WAF1. Hydrangenol increased the phosphorylation of p38 MAPK without affecting the phosphorylation of ERK and JNK. In addition, hydrangenol significantly inhibited the migratory and invasive activities of EJ cells by suppressing the enzymatic activity of MMP-9. Electrophoretic mobility shift assays suggested that the inhibition of MMP-9 activity by hydrangenol was attributable to its suppression of the Sp-1 transcription factor binding activity. This study is the first report on the mode of action of hydrangenol as an inhibitor of bladder cancer. We believe that these results provide novel insights that could aid the development of hydrangenol-based chemotherapeutic agents.

KEYWORDS

MMP-9; hydrangenol; invasion; migration; proliferation

Title

Hydrangenol inhibits the proliferation, migration, and invasion of EJ bladder cancer cells via p21WAF1-mediated G1-phase cell cycle arrest, p38 MAPK activation, and reduction in Sp-1-induced MMP-9 expression.

Author

Shin SS1, Ko MC2, Park YJ3, Hwang B3, Park SL3, Kim WJ4, Moon SK3.

PMID

27032067

Abstract

We previously demonstrated the anti-inflammatory effect of water extract of Hydrangea macrophylla in lipopolysaccharide (LPS)-stimulated macrophage cells. Here, we investigated whether hydrangenol, a bioactive component of H. macrophylla, attenuates the expression of nitric oxide (NO) and its associated gene, inducible NO synthase (iNOS), in LPS-stimulated BV2 microglial cells. Our data showed that low dosages of hydrangenol inhibited LPS-stimulated NO release and iNOS expression without any accompanying cytotoxicity. Hydrangenol also suppressed LPS-induced nuclear translocation of nuclear factor-κB (NF-κB) subunits, consequently inhibiting DNA-binding activity of NF-κB. Additionally, the NF-κB inhibitors, pyrrolidine dithiocarbamate (PDTC) and PS-1145, significantly attenuated LPS-induced iNOS expression, indicating that hydrangenol-induced NF-κB inhibition might be a key regulator of iNOS expression. Furthermore, our data showed that hydrangenol suppresses NO production by inducing heme oxygenase-1 (HO-1). The presence of cobalt protoporphyrin, a specific HO-1 inducer, potently suppressed LPS-induced NO production. Hydrangenol also promoted nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and subsequently increased its binding activity at the specific antioxidant response element sites. Additionally, transient knockdown of Nrf2 significantly downregulated hydrangenol-induced HO-1 expression, indicating that hydrangenol-induced Nrf2 is an upstream regulator of HO-1. Taken together, these data suggest that hydrangenol attenuates NO production and iNOS expression in LPS-stimulated BV2 microglial cells by inhibiting NF-κB activation and by stimulating the Nrf2-mediated HO-1 signaling pathway. Therefore, hydrangenol is a promising therapeutic agent for treatment of LPS-mediated inflammatory diseases.

Copyright ? 2016 Elsevier B.V. All rights reserved.

KEYWORDS

Heme oxygenase-1; Hydrangenol; Nitric oxide; Nuclear factor erythroid 2-related factor 2; Nuclear factor-κB

Title

Hydrangenol inhibits lipopolysaccharide-induced nitric oxide production in BV2 microglial cells by suppressing the NF-κB pathway and activating the Nrf2-mediated HO-1 pathway.

Author

Kim HJ1, Kang CH2, Jayasooriya RGPT1, Dilshara MG1, Lee S1, Choi YH3, Seo YT4, Kim GY5.

Publish date

2016 Jun