We Offer Worldwide Shipping
Login Wishlist

Eleutheroside B

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-E1005

  • Specification : 98%

  • CAS number : 118-34-3

  • Formula : C17H24O9

  • Molecular Weight : 372.37

  • PUBCHEM ID : 5316860

  • Volume : 20mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-E1005

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

372.37

Appearance

White crystalline powder

Botanical Source

Peucedanum praeruptorum,Cirsium japonicum,Akebia quinata,Buddleja officinalis,Atractylodes lancea

Structure Type

Phenylpropanoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC(=CC(=C1OC2C(C(C(C(O2)CO)O)O)O)OC)C=CCO

Synonyms

β-D-Glucopyranoside, 4-(3-hydroxy-1-propenyl)-2,6-dimethoxyphenyl/Sinapyl 4-O-β-D-glucopyranoside alcohol/4-[(1E)-3-Hydroxy-1-propen-1-yl]-2,6-dimethoxyphenyl β-D-glucopyranoside/4-[(1E)-3-Hydroxyprop-1-en-1-yl]-2,6-dimethoxyphenyl β-D-glucopyranoside/β-D-Glucopyranoside, 4-(3-hydroxy-1-propenyl)-2,6-dimethoxyphenyl, (E)-/Ligustrin/Syringin/LILACIN/4-[(1E)-3-Hydroxyprop-1-en-1-yl]-2,6-dimethoxyphenyl-β-D-glucopyranoside/Sinapyl alcohol 4-O-glucoside/β-D-Glucopyranoside, 4-[(1E)-3-hydroxy-1-propenyl]-2,6-dimethoxyphenyl/4-(3-Hydroxypropenyl)-2,6-dimethoxyphenyl-D-glucoside/Methoxyconiferine/β-D-Glucopyranoside, 4-[(1E)-3-hydroxy-1-propen-1-yl]-2,6-dimethoxyphenyl

IUPAC Name

(2R,3S,4S,5R,6S)-2-(hydroxymethyl)-6-[4-[(E)-3-hydroxyprop-1-enyl]-2,6-dimethoxyphenoxy]oxane-3,4,5-triol

Density

1.4±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

342.4±31.5 °C

Boiling Point

642.6±55.0 °C at 760 mmHg

Melting Point

192°C

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#:118-34-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30990939

Abstract

Eleutheroside B (EB) is a phenylpropanoid glycoside with anti-inflammatory properties, neuroprotective abilities, immunomodulatory effects, antinociceptive effects, and regulation of blood glucose. The aim of this study was to investigate the effects of EB on the barrier function in the intestinal porcine epithelial cells J2 (IPEC-J2). The IPEC-J2 cells were inoculated into 96-well plates at a density of 5 × 103 cells per well for 100% confluence. The cells were cultured in the presence of EB at concentrations of 0, 0.05, 0.10, and 0.20 mg/ml for 48 hr. Then, 0.10 mg/ml was selected as the suitable concentration for the estimation of transepithelial electric resistance (TEER) value, alkaline phosphatase activity, proinflammatory cytokines mRNA expression, tight junction mRNA and protein expression. The results of this study indicated that the supplementation of EB in IPEC-J2 cells decreased cellular membrane permeability and mRNA expression of proinflammatory cytokines, including interleukin-6 (IL-6), interferon-γ (INF-γ), and tumour necrosis factor-α (TNF-α). The supplementation of EB in IPEC-J2 cells increased tight junction protein expression and anti-inflammatory cytokines, interleukin 10 (IL-10) and transforming growth factor beta (TGF-β). In addition, the western blotting and real-time quantitative polymerase chain reaction (RT-qPCR) results indicated that EB significantly (p < 0.05) increased the mRNA and protein expression of intestinal tight junction proteins, Claudin-3, Occludin, and Zonula Occludins protein-1 (ZO-1). Therefore, dietary supplementation of EB may increase intestinal barrier function, tight junction protein expression, anti-inflammatory cytokines, and decrease proinflammatory cytokines synthesis in IPEC-J2 cells.

KEYWORDS

TEER; anti-inflammatory cytokines; eleutheroside B; intestinal epithelial permeability; tight junction proteins.

Title

Eleutheroside B Increase Tight Junction Proteins and Anti-Inflammatory Cytokines Expression in Intestinal Porcine Jejunum Epithelial Cells (IPEC-J2)

Author

Dongsheng Che 1 2 , Bao Zhao 1 2 , Yueli Fan 1 2 , Rui Han 1 2 , Chun Zhang 3 , Guixin Qin 1 2 , Seidu Adams 1 2 , Hailong Jiang 1 2

Publish date

2019 Jul

PMID

31661774

Abstract

Acute kidney injury (AKI) is a common, complex, and severe clinical syndrome characterized by rapid decline in renal function, combined with tissue damage. Currently, the prevention and treatment of AKI are focused on symptomatic treatment, rather than treating the underlying causes. Therefore, there is no specific treatment to prevent renal injury except for renal dialysis. In this study, we used cisplatin-induced AKI mouse and human kidney-2 (HK-2) cell models to evaluate the renal protective effect of eleutheroside B, an active compound in traditional Chinese medicines. MTT assay was used to detect the effect of eleutheroside B on proliferation of human HK-2 cells in presence and in absence of cisplatin. Western blot and immunostaining were used to detect the protein level of kidney injury molecule-1 (KIM-1), cleaved caspase-3, receptor-interacting protein kinase (RIPK)-1, and RIPK-3. Real-time PCR was used to detect the mRNA levels of chemokines (like monocyte chemotactic protein 1, MCP-1) and pro-inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor (TNF-α). Flow cytometry assay was used to detect apoptosis of HK-2 cells. In vivo results showed that eleutheroside B reduced the increase in serum creatinine and blood urea nitrogen (BUN) levels in the AKI model. Periodic acid-Schiff staining and Western blot analysis of KIM-1 showed that eleutheroside B alleviated tubular cell injury. Further, eleutheroside B reduced macrophage infiltration and production of inflammatory cytokines, inhibited the activation of nuclear factor (NF)-κB, and inhibited apoptosis and programmed necrosis. The mechanism may be that eleutheroside B can activate the insulin-like growth factor (IGF) pathway and its downstream pathway by downregulating the expression of IGFBP-7, thus promoting cell proliferation. Therefore, our results suggest that eleutheroside B is a potential drug for AKI treatment.

KEYWORDS

IGFBP-7; acute kidney injury; apoptosis; cisplatin; eleutheroside B; inflammation; programmed necroptosis.

Title

Eleutheroside B Protects Against Acute Kidney Injury by Activating IGF Pathway

Author

Hongmei Zang 1 2 3 , Qin Yang 4 , Jun Li 5 6 7

Publish date

2019 Oct 28

PMID

25206404

Abstract

Eleutheroside B or E, the main component of Acanthopanax, can relieve fatigue, enhance memory, and improve human cognition. Numerous studies have confirmed that high doses of acetylcholine significantly attenuate clinical symptoms and delay the progression of Alzheimer’s disease. The present study replicated a rat model of aging induced by injecting quinolinic acid into the hippocampal CA1 region. These rats were intraperitoneally injected with low, medium and high doses of eleutheroside B or E (50, 100, 200 mg/kg), and rats injected with Huperzine A or PBS were used as controls. At 4 weeks after administration, behavioral tests showed that the escape latencies and errors in searching for the platform in a Morris water maze were dose-dependently reduced in rats treated with medium and high-dose eleutheroside B or E. Hematoxylin-eosin staining showed that the number of surviving hippocampal neurons was greater and pathological injury was milder in three eleutheroside B or E groups compared with model group. Hippocampal homogenates showed enhanced cholinesterase activity, and dose-dependent increases in acetylcholine content and decreases in choline content following eleutheroside B or E treatment, similar to those seen in the Huperzine A group. These findings indicate that eleutheroside B or E improves learning and memory in aged rats. These effects of eleutheroside B or E may be mediated by activation of cholinesterase or enhanced reuse of choline to accelerate the synthesis of acetylcholine in hippocampal neurons.

KEYWORDS

Huperzine A; acetylcholine; aged rats; choline; cholinesterase; eleutheroside B or E; grants-supported paper; hippocampus; learning and memory; mechanism; neural regeneration; neuroregeneration; quinolinic acid; traditional Chinese medicine.

Title

Eleutheroside B or E Enhances Learning and Memory in Experimentally Aged Rats

Author

Debin Huang 1 , Zehua Hu 1 , Zhaofen Yu 1 4

Publish date

2013 Apr 25


Description :

Syringin may exert sleep-potentiating effects through the NOS/NO pathway PUMID/DOI:25377727 Fundam Clin Pharmacol. 2015 Apr;29(2):178-84. Syringin significantly reduced NO concentration and NOS activity. Administration of l-Arg prolonged sleep latency and shortened sleep duration, and the effects were fully reversed by Syringin coadministration. Administration of L-NAME induced a significant reduction in sleep latency and a corresponding increase in sleep duration, and coadministration of Syringin further enhanced the effects. The finding of our study demonstrated that Syringin could exert sleep-potentiating effects on anesthetized mice in a time- and dose-dependent manner, and these effects may be intimately correlated with the NO/NOS pathway. Syringin from stem bark of Fraxinus rhynchophylla protects Abeta(25-35)-induced toxicity in neuronal cells. PUMID/DOI:20422361 Arch Pharm Res. 2010 Apr;33(4):531-8. When the neuroblastoma cells were exposed to 50 microM Abeta(25-35), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction rate (survival rate) decreased to 60.21 +/- 2.16% over control while Syringin treated ones recovered cell viability up to 79.12 +/- 1.39% at 20 microM. In addition, 20 microM Syringin almost completely removed Abeta(25-35)-induced reactive oxygen species. The neuroprotective effect of Syringin seemed to be originated from the reduction of apoptosis since decrease in caspase-3 activity and expression, reduction in cleaved PARP, and DNA fragmentation were observed. These results suggest that F. rhynchophylla and Syringin are expected to be useful for preventing Abeta(25-35)-induced neuronal cell damage. Anti-inflammatory and antinociceptive effects of sinapyl alcohol and its glucoside syringin. PUMID/DOI:15549657 Planta Med. 2004 Nov;70(11):1027-32. In the present study, Syringin, isolated by activity-guided fractionation of the ethyl acetate (EtOAc) extracts of the stem bark of Magnolia sieboldii, and sinapyl alcohol, the hydrolysate of Syringin, were evaluated for anti-inflammatory and antinociceptive activities. Sinapyl alcohol (20, 30 mg/kg/day, p. o.) inhibited increased vascular permeability by acetic acid in mice and reduced acute paw edema by carrageenan in rats more so than Syringin. When analgesic activity was measured using the acetic acid-induced writhing test and the hot plate test, sinapyl alcohol was much more potent than Syringin in a mouse model. In addition, sinapyl alcohol more potently inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor (TNF)-alpha production by macrophages than Syringin. Consistent with these observations, the expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 was reduced by sinapyl alcohol in a concentration-dependent manner. These results suggest that the anti-inflammatory and antinociceptive effects of Syringin after oral administration may be attributed to its in vivo transformation to sinapyl alcohol.