We Offer Worldwide Shipping
Login Wishlist

Hederagenin

$78

  • Brand : BIOFRON

  • Catalogue Number : BF-H3003

  • Specification : 98%

  • CAS number : 465-99-6

  • Formula : C30H48O4

  • Molecular Weight : 472.7

  • PUBCHEM ID : 73299

  • Volume : 20mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-H3003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

472.7

Appearance

White crystalline powder

Botanical Source

Paeonia suffruticosa,Akebia quinata,Aquilaria sinensis,Boehmeria nivea,Momordica subangulata subsp. renigera

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1(CCC2(CCC3(C(=CCC4C3(CCC5C4(CCC(C5(C)CO)O)C)C)C2C1)C)C(=O)O)C

Synonyms

Olean-12-en-28-oic acid, 3,23-dihydroxy-, (3β)-/(3beta,4alpha)-3,23-Dihydroxyolean-12-en-28-oic acid/(4aS,6aS,6bR,8aR,9R,10S,12aR,12bR,14bS)-10-Hydroxy-9-(hydroxymethyl)-2,2,6a,6b,9,12a-hexamethyl-1,3,4,5,6,6a,6b,7,8,8a,9,10,11,12,12a,12b,13,14b-octadecahydro-4a(2H)-picenecarboxylic acid/Hederagenol/Astrantiagenin E/3,23-dihydroxyolean-12-en-28-oic acid/Caulosapogenin/Hederagenic acid/Hederagenin/Melanthigenin/3,23-Dihydroxyolean-12-en-28-acid/(3b,4a)-3,23-Dihydroxyolean-12-en-28-oic Acid/23-hydroxyoleanolic acid/(3β)-3,23-Dihydroxyolean-12-en-28-oic acid

IUPAC Name

(4aS,6aR,6aS,6bR,8aR,9R,10S,12aR,14bS)-10-hydroxy-9-(hydroxymethyl)-2,2,6a,6b,9,12a-hexamethyl-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid

Density

1.1±0.1 g/cm3

Solubility

Methanol

Flash Point

324.3±26.6 °C

Boiling Point

589.4±50.0 °C at 760 mmHg

Melting Point

332 - 334ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2918190000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:465-99-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26481049

Abstract

Clematis mandshurica Ruprecht root has been used in Asia as a traditional anti-inflammatory, analgesic, and antitumor agent. Its main active component is hederagenin, a naturally occurring triterpene, and in this study, we examined the anti-inflammatory effects of hederagenin in lipopolysaccharide-stimulated RAW 264.7 cells using an enzyme-linked immunosorbent assay, Western blot, and RT-PCR. In addition, its effects on acute inflammation in vivo were observed using a carrageenan-induced mouse hind paw edema assay. Furthermore, the changes on the histopathology and histomorphometry of hind paw skins were examined using carrageenan-treated mice. Treatment with hederagenin (10, 30 and 100μM) resulted in inhibited levels of protein expression of lipopolysaccharide-stimulated iNOS, COX-2, and NF-κB as well as production of NO, PGE2, TNF-α, IL-1β, and IL-6 induced by lipopolysaccharide. Consistent with these results, hederagenin also dose-dependently reduced the lipopolysaccharide-induced mRNA levels of iNOS and COX-2, and of the above-mentioned cytokines. Interestingly, results of the carrageenan-induced mouse hind paw edema assay showed an anti-edema effect of hederagenin. Furthermore, hederagenin (30mg/kg) inhibited the carrageenan-induced increases in skin thicknesses, infiltrated inflammatory cells, and mast cell degranulation. These results suggest that hederagenin may possess anti-inflammatory activities.

KEYWORDS

Hederagenin; Histological examination; Inflammatory response; Mouse paw edema; Nuclear factor-kappa B.

Title

Hederagenin, a Major Component of Clematis Mandshurica Ruprecht Root, Attenuates Inflammatory Responses in RAW 264.7 Cells and in Mice

Author

Chul Won Lee 1 , Sang Mi Park 2 , Rongjie Zhao 3 , Chu Lee 4 , Wonjoo Chun 5 , Yonghae Son 5 , Sung Hun Kim 6 , Ji Yun Jung 2 , Kyung Hwan Jegal 2 , Il Je Cho 2 , Sae Kwang Ku 2 , Young Woo Kim 2 , Seong A Ju 7 , Sang Chan Kim 8 , Won G An 9

Publish date

2015 Dec 7

PMID

28067819

Abstract

In this study, we determined the effects of hederagenin isolated from Akebia quinata fruit on alcohol-induced hepatotoxicity in rats. Specifically, we investigated the hepatoprotective, anti-inflammatory, and anti-apoptotic effects of hederagenin, as well as the role of AKT and mitogen-activated protein kinase (MAPK) signaling pathways in ethanol-induced liver injury. Experimental animals were randomly divided into three groups: normal (sham), 25% ethanol, and 25% ethanol + hederagenin (50 mg/kg/day). Each group was orally administered the respective treatments once per day for 21 days. Acetaldehyde dehydrogenase-2 mRNA expression was higher and alcohol dehydrogenase mRNA expression was lower in the ethanol + hederagenin group than those in the ethanol group. Pro-inflammatory cytokines, including TNF-α, IL-6, and cyclooxygenase-2, significantly increased in the ethanol group, but these increases were attenuated by hederagenin. Moreover, Western blot analysis showed increased expression of the apoptosis-associated protein, Bcl-2, and decreased expression of Bax and p53 after treatment with hederagenin. Hederagenin treatment attenuated ethanol-induced increases in activated p38 MAPK and increased the levels of phosphorylated AKT and ERK. Hederagenin alleviated ethanol-induced liver damage through anti-inflammatory and anti-apoptotic activities. These results suggest that hederagenin is a potential candidate for preventing alcoholic liver injury.

KEYWORDS

Hederagenin; Histological examination; Inflammatory response; Mouse paw edema; Nuclear factor-kappa B.

Title

Hederagenin Supplementation Alleviates the Pro-Inflammatory and Apoptotic Response to Alcohol in Rats

Author

Gyeong-Ji Kim 1 , Da Hye Song 2 , Han Seok Yoo 3 , Kang-Hyun Chung 4 , Kwon Jai Lee 5 , Jeung Hee An 6

Publish date

2017 Jan 6

PMID

29456786

Abstract

Acquired resistance to cisplatin is the most common reason for the failure of cisplatin chemotherapy. Hederagenin, triterpenoids extracted from ivy leaves, exhibits antitumor activity in various types of cancer. However, the therapeutic potential of hederagenin in head and neck cancer (HNC) has remained unclear. Therefore, we examined the effects of hederagenin in cisplatin-resistant HNC cells and characterized its molecular mechanisms of action in this context. We evaluated the effects of hederagenin treatment on cell viability, apoptosis, reactive oxygen species (ROS) production, glutathione levels, mitochondrial membrane potential (ΔΨm), and protein and mRNA expression in HNC cells. The antitumor effect of hederagenin in mouse tumor xenograft models was also analyzed. Hederagenin selectively induced cell death in both cisplatin-sensitive and cisplatin-resistant HNC cells by promoting changes in ΔΨm and inducing apoptosis. Hederagenin inhibited the Nrf2-antioxidant response element (ARE) pathway and activated p53 in HNC cells, thereby enhancing ROS production and promoting glutathione depletion. These effects were reversed by the antioxidant trolox. Hederagenin activated intrinsic apoptotic pathways via cleaved PARP, cleaved caspase-3, and Bax. The selective inhibitory effects of hederagenin were confirmed in cisplatin-resistant HNC xenograft models. These data suggest that hederagenin induces cell death in resistant HNC cells via the Nrf2-ARE antioxidant pathway.

Title

Hederagenin Induces Apoptosis in Cisplatin-Resistant Head and Neck Cancer Cells by Inhibiting the Nrf2-ARE Antioxidant Pathway

Author

Eun Hye Kim 1 , Seungho Baek 2 , Daiha Shin 1 , Jaewang Lee 1 , Jong-Lyel Roh 1

Publish date

2017


Description :

Hederagenin is a triterpenoid saponin. It can inhibit LPS-stimulated expression of iNOS, COX-2, and NF-κBHederagenin can Exhibits multiple pharmacological activities in the treatment of hyperlipidemia, antilipid peroxidation, antiplatelet aggregation, liver protection, antidepression, anti-inflammation.[1]In vitro:1) Hederagenin can correct the imbalance of endothelial function by inhibiting the release of large amounts of iNOS and increasing eNOS contents and inhibits the IKKβ/NF-κB signaling pathway to reduce the release of IL-6, IFN-γ, TNF-α, and other inflammatory factors. [1]2) The EC50 of hederagenin is 39 ± 6 μM in A549 cancer cell line, but it's inactive for DLD-1 cells. [2]3) Hederagenin inhibited LPS-induced production of NO, PGE2and cytokines in cells.[3]4) Hederagenin had an anti-edema effect on the CA-induced mouse hind paw edema assay. [3]5) Hederagenin inhibited the CA-induced increase in skin thicknesses. [3]In vivo: The rats in the hederagenin group were administered hederagenin at 20 mg/kg/d via gavage.(More details please refer to the protocol below). In AS rat models induced by a high-lipid diet plus VD3, hederagenin can effectively reduce serum lipid, ALT, and AST levels, in addition to improving liver function, relieving high blood coagulation, and slowing blood flow and stasis by improving blood rheology. [1]