Hydrangenol

CAS# 480-47-7

Hydrangenol

2D Structure

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Quality Control of Hydrangenol

3D structure

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Hydrangenol

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Chemical Properties of Hydrangenol

Cas No. 480-47-7 SDF Download SDF
PubChem ID 119199 Appearance Powder
Formula C15H12O4 M.Wt 256.3
Type of Compound Flavonoids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 8-hydroxy-3-(4-hydroxyphenyl)-3,4-dihydroisochromen-1-one
SMILES C1C(OC(=O)C2=C1C=CC=C2O)C3=CC=C(C=C3)O
Standard InChIKey DGKDFNDHPXVXHW-UHFFFAOYSA-N
Standard InChI 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
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Hydrangenol

The herbs of Hydrangea hortensia

Biological Activity of Hydrangenol

Description1. Hydrangenol is a strong contact sensitizer found in hydrangea (Hydrangea sp.; Hydrangeaceae). 2. Hydrangenol can significantly inhibit the passive cutaneous anaphylaxis (PCA) reaction, it has antiallergic activity. 3. Hydrangenol has anti-inflammatory activity,it can attenuate NO production and inducible NO synthase expression in lipopolysaccharide (LPS)-stimulated BV2 microglial cells by inhibiting NF-κB activation and by stimulating the Nrf2-mediated HO-1 signaling pathway. 4. Hydrangenol has antifungal activity.
TargetsNO | NOS | NF-kB | HO-1 | Nrf2 | Antifection

Hydrangenol Dilution Calculator

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Hydrangenol Molarity Calculator

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Preparing Stock Solutions of Hydrangenol

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.9017 mL 19.5084 mL 39.0168 mL 78.0336 mL 97.5419 mL
5 mM 0.7803 mL 3.9017 mL 7.8034 mL 15.6067 mL 19.5084 mL
10 mM 0.3902 mL 1.9508 mL 3.9017 mL 7.8034 mL 9.7542 mL
50 mM 0.078 mL 0.3902 mL 0.7803 mL 1.5607 mL 1.9508 mL
100 mM 0.039 mL 0.1951 mL 0.3902 mL 0.7803 mL 0.9754 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Hydrangenol

Effects of phyllodulcin, hydrangenol, and their 8-O-glucosides, and thunberginols A and F from Hydrangea macrophylla SERINGE var. thunbergii MAKINO on passive cutaneous anaphylaxis reaction in rats.[Pubmed:10480329]

Biol Pharm Bull. 1999 Aug;22(8):870-2.

We examined the antiallergic effects of phyllodulcin, Hydrangenol, and their 8-O-glucosides, and thunberginols A and F isolated from the processed leaves (Hydrangeae Dulcis Folium) and dried leaves of Hydrangea macrophylla SERINGE var. thunbergii MAKINO using the passive cutaneous anaphylaxis (PCA) reaction. With the exception of phyllodulcin, these constituents were found to significantly inhibit the PCA reaction. Although thunberginol A showed the most potent inhibitory effect, Hydrangenol was considered to be the principal antiallergic component in the processed leaves, after taking into account their contents.

Hydrangenol inhibits lipopolysaccharide-induced nitric oxide production in BV2 microglial cells by suppressing the NF-kappaB pathway and activating the Nrf2-mediated HO-1 pathway.[Pubmed:27032067]

Int Immunopharmacol. 2016 Jun;35:61-69.

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-kappaB (NF-kappaB) subunits, consequently inhibiting DNA-binding activity of NF-kappaB. Additionally, the NF-kappaB inhibitors, pyrrolidine dithiocarbamate (PDTC) and PS-1145, significantly attenuated LPS-induced iNOS expression, indicating that Hydrangenol-induced NF-kappaB 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-kappaB 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.

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