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Rhein

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-R3002

  • Specification : 98%

  • CAS number : 478-43-3

  • Formula : C15H8O6

  • Molecular Weight : 284.22

  • PUBCHEM ID : 10168

  • Volume : 25mg

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Catalogue Number

BF-R3002

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

284.22

Appearance

Yellow crystalline powder

Botanical Source

Rheum palmatum,Reynoutria japonica,Fallopia multiflora,Dendrobium fimbriatum,Rheum wittrockii

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC2=C(C(=C1)O)C(=O)C3=C(C2=O)C=C(C=C3O)C(=O)O

Synonyms

Rhein/1,8-dihydroxy-3-carboxy-9,10-anthraquinone/Cassic acid/2-Anthracenecarboxylic acid, 9,10-dihydro-4,5-dihydroxy-9,10-dioxo-/Rheic acid/Rhubarb Yellow/1,8-dihydroxyanthraquinone-3-carboxylic acid/1,8-dihydroxy-3-carboxyanthraquinone/9,10-Dihydro-4,5-dihydroxy-9,10-dioxo-2-anthracenecarboxylic acid/Monorhein/4,5-dihydroxy-9,10-dioxo-9,10-dihydroanthracene-2-carboxylic acid/4,5-Dihydroxy-9,10-dioxo-9,10-dihydro-2-anthracenecarboxylic acid/4,5-Dihydroxyanthraquinone-2-carboxylic acid/9,10-dihydro-4,5-dihydroxy-9,10-dioxoanthracene-2-carboxylic acid/Chrysazin-3-carboxylic acid

IUPAC Name

4,5-dihydroxy-9,10-dioxoanthracene-2-carboxylic acid

Density

1.7±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate

Flash Point

329.4±26.6 °C

Boiling Point

597.8±50.0 °C at 760 mmHg

Melting Point

≥300 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2918990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:478-43-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30466606

Abstract

BACKGROUND:
Rhein, an anthraquinone compound isolated from rhubarb, has been shown to protect the pancreatic β cells from hyperglycemia induced apoptosis in our previous studies.
PURPOSE:
In the present study, we examined whether rhein can protect myocardial cells against ischemia reperfusion (I/R)-induced apoptosis and investigated the underlying mechanism.
METHODS:
We used an in vitro model of myocardial hypoxia/reoxygenation (H/R) injury. H9c2 cells were incubated with rhein for 1 h and then subjected to hypoxia for 6 h, followed by reoxygenation for 2 h. Cells viability, apoptosis and ROS were assayed for the treated cells. AKT, p-AKT, GSK3β, p- GSK3β, P38 and p-P38 proteins were analyzed using Western blotting. PI3K/AKT inhibitor, LY294002, and GSK3β siRNA were also used to determine the signaling pathways involved in the protection by rhein.
RESULTS:
Rhein increased viability, decreased apoptosis and ROS production, of the cells that were exposed to H/R. Rhein also increased the phosphorylation of AKT and GSK3β, an effect that was eliminated by LY294002. GSK3β silencing by siRNA showed similar effect as LY294002. The p-P38 level was upregulated by H/R and downregulated in the presence of rhein; however, the p-P38 downregulation was completely abolished by GSK3β silencing.
CONCLUSION:
Rhein protects myocardial H9c2 cells against hypoxia/reoxygenation induced injury via AKT/ GSK3β/p38 pathway.
Copyright © 2018. Published by Elsevier GmbH.

KEYWORDS

H9c2 cells; Hypoxia/reoxygenation; Myocardial cells; PI3K/AKT; Rhein

Title

Rhein protects the myocardiac cells against hypoxia/reoxygention-induced injury by suppressing GSK3β activity.

Author

Liu J1, Li Y1, Tang Y1, Cheng J1, Wang J1, Li J1, Ma X1, Zhuang W1, Gong J2, Liu Z3.

Publish date

2018 Dec 1

PMID

28652704

Abstract

Rhein is an important component in traditional Chinese herbal medicine formulations for gastrointestinal disorders, including inflammatory bowel diseases such as ulcerative colitis. In this study, we investigated the beneficial effects of rhein in inflammation models in the transgenic zebrafish line TG (corolla eGFP), in which both macrophages and neutrophils express eGFP and RAW264.7 macrophages. We found that the tail-cutting-induced migration of immune cells was significantly reduced in transgenic zebrafish treated with rhein. In addition, the production of proinflammatory cytokines, including IL-6, IL-1β, and tumor necrosis factor-α, were significantly reduced in lipopolysaccharide (LPS)-induced RAW264.7 macrophages treated with rhein. Parallel to the inhibition of proinflammatory cytokines, rhein significantly reduced phosphorylation levels of NF-κB p65 and inducible nitric oxide synthase, as well as COX-2 protein expression levels. Furthermore, rhein significantly reduced NALP3 and cleaved IL-1β expression in LPS + ATP-induced RAW264.7 macrophages. Thus, the present study demonstrates that rhein may exhibit its anti-inflammatory action via inhibition of NF-κB and NALP3 inflammasome pathways.

KEYWORDS

COX-2; NALP3; NF-κB; iNOS; inflammatory; rhein; zebrafish

Title

Rhein attenuates inflammation through inhibition of NF-κB and NALP3 inflammasome in vivo and in vitro.

Author

Ge H1, Tang H2, Liang Y2, Wu J2, Yang Q2, Zeng L2, Ma Z2.

Publish date

2017 Jun 6

PMID

26419468

Abstract

Background: Rhein (1,8-dihydroxy-3-carboxyanthraquinone) is a monomer of anthraquinone derivatives mainly found in Polygonaceae plants such as Rhubarb, and Cuspidatum, widely used in the traditional Chinese medicine with many pharmacological activities, such as antitumor, anti-inflammatory and antifibrotic effects, and regulation of glucose and lipid metabolism.
Objective: To conclude the role of Rhein in cancer control and its mechanisms for its futher deep research and potential clinical application.
Method: All kinds of reports previously related to Rhein from PubMed datebase were collected, integrated and analyzed.
Results: Rhein could control many cancer cells by regulating their proliferation and apoptosis, invasion and migration, especially intrinsic and extrinsic apoptosis pathways induced by Rhein plays the core role in cancer control. For good inhibitory role in NF-κB pathway, the Ras/Raf/MEK (MAPK)/ERK and PTEN/PI3K/AKT/mTOR pathways are other two key pathways regulated by Rhein with its role in antiphosphorylation of ERK, PI3K and AKT to control many cancers’ development which frequently dysregulated in cancer, involved in the activation, proliferation, invasion, and migration of cancer cells.
Conclusion: Rhein is a potential cancer treatment agent.
Keywords: Angiogenesis; anthraquinone; antitumor; apoptosis; invasion; migration; proliferation; rhein.
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Title

Research Progress on the Antitumor Effects of Rhein: Literature Review

Author

Chao Wu 1 , Hongyan Cao 1 , Hua Zhou 1 , Lin Sun 2 , Jingui Xue 1 , Jianyuan Li 1 , Yanqin Bian 3 , Runfei Sun 1 , Shu Dong 3 , Ping Liu 1 , Mingyu Sun 1

Publish date

2017;


Description :

Rhein is a lipophilic anthraquinone extensively found in medicinal herbs, and has many pharmacological effects, including epatoprotective, nephroprotective, anti-inflammatory, antioxidant, anticancer, and antimicrobial activities. IC50 value:Target:In vitro: Rhein (0.1 and 1 mg/mL) evidently suppressed cell proliferation and mitogen-activated protein (MAP) kinase activation in human colon adenocarcinoma cells (Caco-2) but significantly lessened H2O2-induced DNA damage and the elevated MDA and ROS levels induced by H2O2/Fe2+ at the concentrations of 0.1-10 mg/mL [1].In vivo: Oral administration of rhein (150 mg/kg/d) evidently ameliorated renal interstitial fibrotic lesions and attenuated the expression of α-SMA and deposition of fibronectin (FN) in mice with renal interstitial fibrosis induced by unilateral ureteral obstruction. Rhein also suppressed TGF-β1 and its type I receptor expression in obstructed kidneys [1]. The biochemical parameters results of IgAN model rats showed that rhein-prevented and rhein-treated both improved the biochemical parameters and relieved renal pathological injury. The expressions of renal tissue TLR4, TGF-β1, but not TLR9 were significantly elevated in IgAN model rats (P < 0.05). Rhein-prevented and rhein-treated both inhibited TLR4 and TGF-β1 expressions [2].