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Rhapontin

$78

  • Brand : BIOFRON

  • Catalogue Number : BF-R1003

  • Specification : 98%

  • CAS number : 155-58-8

  • Formula : C21H24O9

  • Molecular Weight : 420.41

  • PUBCHEM ID : 637213

  • Volume : 20mg

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Catalogue Number

BF-R1003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

420.41

Appearance

Yellow crystall

Botanical Source

Rheum palmatum,Alternanthera philoxeroides,Commelina communis,Rheum hotaoense

Structure Type

Stilbenes

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C=C(C=C1)C=CC2=CC(=CC(=C2)OC3C(C(C(C(O3)CO)O)O)O)O)O

Synonyms

3-Hydroxy-5-[2-(3-hydroxy-4-melhoxyphenyl)ethenyl]phenyl b-D-Glucopyranoside/3-hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenyl β-D-glucopyranoside/Rhapontin/Rhaponticin/Rhaponiticin/RHAPONTIN,TECH./β-D-Glucopyranoside, 3-hydroxy-5-(2-(3-hydroxy-4-methoxyphenyl)ethenyl)phenyl (9CI)/3-Hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)vinyl]phenyl-β-D-glucopyranoside/(2S,3R,4S,5S,6R)-2-{3-Hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)vinyl]phenoxy}-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/3-Hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)vinyl]phenyl β-D-glucopyranoside/4'-Methoxy-3,3',5-stilbenetriol 3-Glucoside/β-D-Glucopyranoside de 3-hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenyle/trans-Rhapontin/β-D-Glucopyranoside, 3-hydroxy-5-[2- (3-hydroxy-4-methoxyphenyl)ethenyl]phenyl/(2S,3R,4S,5S,6R)-2-{3-Hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenoxy}-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/β-D-Glucopyranoside, 3-hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenyl/RHAMNOSE,L-(+)-(P)/β-D-Glucopyranoside, 3-hydroxy-5-[2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenyl/3-hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)vinyl]phenyl β-glucopyranoside/Ponticin

IUPAC Name

(2S,3R,4S,5S,6R)-2-[3-hydroxy-5-[(E)-2-(3-hydroxy-4-methoxyphenyl)ethenyl]phenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Density

1.5±0.1 g/cm3

Solubility

Methanol; DMSO

Flash Point

406.9±32.9 °C

Boiling Point

749.3±60.0 °C at 760 mmHg

Melting Point

236-240ºC

InChl

InChI=1S/C21H24O9/c1-28-16-5-4-11(8-15(16)24)2-3-12-6-13(23)9-14(7-12)29-21-20(27)19(26)18(25)17(10-22)30-21/h2-9,17-27H,10H2,1H3/b3-2+/t17-,18-,19+,20-,21-/m1/s1

InChl Key

GKAJCVFOJGXVIA-DXKBKAGUSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:155-58-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

27930969

Abstract

Rhapontin (3, 3′, 5-trihydroxy-4′-methoxystilbene-3-O-glucoside) has anti-thrombotic, anti-allergic and anti-diabetic activities. This study aimed to assess the protective effects of rhapontin on intestinal damage in vivo and in vitro. In a dextran sodium sulfate (DSS)-induced mouse model, oral administration of rhapontin (100mg/kg) significantly attenuated colonic pathological damage and remarkably inhibited infiltration by inflammatory cells, myeloperoxidase (MPO) activity, NLRP3 inflammasome activation and SIRT1 expression in the colon. Moreover, rhapontin prevented DSS-induced impairment in the colon epithelium barrier by increasing the expression of tight junction proteins, such as zonula occludens-1(ZO-1) and occludin, and reduced apoptosis-associated protein (cyt-c, the ratio of bcl-2/bax and cleaved-capase9) expression in the colon. The in vitro results showed that rhapontin significantly reduced NLRP3 inflammasome activation and cleaved caspase-1 expression as well as lowered IL-1β secretion in LPS-stimulated human-THP-1-derived macrophages. Further study revealed that compound EX257 (an SIRT1 inhibitor) blocked the inhibitory effects of rhapontin on NLRP3-dependent caspase-1 activation and IL-β production in activated macrophages. In addition, in TNF-α-stimulated intestinal epithelial NCM460 cells, rhapontin significantly increased the expressions of occludin and ZO-1 and notably reduced the ratio of bcl-2/bax and cleaved-capase9 expression through SRIT1 signaling. In sum, the protective effect of rhapontin is from blocking the NLRP3 priming cascade reaction and is dependent on SIRT1 activation. Our findings demonstrate that rhapontin might be a potential agent for the treatment of colitis by targeting SIRT1.

KEYWORDS

Inflammation; Intestinal barrier; NLRP3 inflammasome; Rhapontin; SIRT1.

Title

Rhapontin Ameliorates Colonic Epithelial Dysfunction in Experimental Colitis Through SIRT1 Signaling

Author

Wencheng Wei 1 , Lei Wang 1 , Kai Zhou 1 , Haifeng Xie 2 , Mian Zhang 1 , Chaofeng Zhang 3

Publish date

2017 Jan

PMID

28364627

Abstract

Background: Pulmonary fibrosis is a scaring process related to chronic lung injury of all causes. The treatment options for pulmonary fibrosis are very limited. Rhapontin has anti-inflammatory effect and anti-proliferative activity which is widely distributed in the medicinal plants of Rheum genus in China. However, the anti-fibrotic activities of rhapontin have not been previously investigated.
Methods: The effect of rhapontin on TGF-β1-mediated extracellular matrix (ECM) deposition in primary lung fibroblast (PLF) cells, on TGF-β1 secretion in LPS-stimulated human THP-1 derived macrophages in vitro, and on bleomycin (BLM)-induced pulmonary fibrosis was investigated in vivo. Fibrotic mice were induced by intratracheal instillation of bleomycin, and then treated with rhapontin (25, 50, or 100mg/kg/day) or prednisone (6.5mg/kg/day, positive drug) for 2weeks.
Results: In TGF-β1 stimulated PLFs, treatment with rhapontin resulted in a reduction of ECM with a decrease in Lox2 and p-Smad2/3. In LPS activated macrophages, treatment with rhapontin reduced TGF-β1 production. However, in vitro the attenuated ECM deposition and inflammatory response by rhapontin were closely associated with AMPK activation, and these suppression of rhapontin were significantly abolished by the AMPK inhibitor. Treatment with rhapontin for 2weeks resulted in an amelioration of the BLM-induced pulmonary fibrosis in rats with a lower Lox2, whereas a higher AMPK expression, with reductions of the pathological score, collagen deposition, TGF-β1, α-SMA, Lox2, and HIF-1α expressions in lung tissues at fibrotic stage at 100mg/kg.
Conclusion: In summary, rhapontin reversed ECM, as well as Lox2 proliferation in vitro and prevented pulmonary fibrosis in vivo by modulating AMPK activation and suppressing the TGF-β/Smad pathway.

KEYWORDS

Inflammation; Intestinal barrier; NLRP3 inflammasome; Rhapontin; SIRT1.

Title

Protective Role of Rhapontin in Experimental Pulmonary Fibrosis in Vitro and in Vivo

Author

Lijun Tao 1 , Juan Cao 1 , Wencheng Wei 1 , Haifeng Xie 2 , Mian Zhang 1 , Chaofeng Zhang 3

Publish date

2017 Jun

PMID

27930969

Abstract

Rhapontin (3, 3′, 5-trihydroxy-4′-methoxystilbene-3-O-glucoside) has anti-thrombotic, anti-allergic and anti-diabetic activities. This study aimed to assess the protective effects of rhapontin on intestinal damage in vivo and in vitro. In a dextran sodium sulfate (DSS)-induced mouse model, oral administration of rhapontin (100mg/kg) significantly attenuated colonic pathological damage and remarkably inhibited infiltration by inflammatory cells, myeloperoxidase (MPO) activity, NLRP3 inflammasome activation and SIRT1 expression in the colon. Moreover, rhapontin prevented DSS-induced impairment in the colon epithelium barrier by increasing the expression of tight junction proteins, such as zonula occludens-1(ZO-1) and occludin, and reduced apoptosis-associated protein (cyt-c, the ratio of bcl-2/bax and cleaved-capase9) expression in the colon. The in vitro results showed that rhapontin significantly reduced NLRP3 inflammasome activation and cleaved caspase-1 expression as well as lowered IL-1β secretion in LPS-stimulated human-THP-1-derived macrophages. Further study revealed that compound EX257 (an SIRT1 inhibitor) blocked the inhibitory effects of rhapontin on NLRP3-dependent caspase-1 activation and IL-β production in activated macrophages. In addition, in TNF-α-stimulated intestinal epithelial NCM460 cells, rhapontin significantly increased the expressions of occludin and ZO-1 and notably reduced the ratio of bcl-2/bax and cleaved-capase9 expression through SRIT1 signaling. In sum, the protective effect of rhapontin is from blocking the NLRP3 priming cascade reaction and is dependent on SIRT1 activation. Our findings demonstrate that rhapontin might be a potential agent for the treatment of colitis by targeting SIRT1.

KEYWORDS

Inflammation; Intestinal barrier; NLRP3 inflammasome; Rhapontin; SIRT1.

Title

Rhapontin Ameliorates Colonic Epithelial Dysfunction in Experimental Colitis Through SIRT1 Signaling

Author

Wencheng Wei 1 , Lei Wang 1 , Kai Zhou 1 , Haifeng Xie 2 , Mian Zhang 1 , Chaofeng Zhang 3

Publish date

2017 Jan


Description :

Rhaponticin from rhubarb rhizomes alleviates liver steatosis and improves blood glucose and lipid profiles in KK/Ay diabetic mice. PUMID/DOI:19235684 Planta Med. 2009 Apr;75(5):472-7. We isolated several stilbene compounds including rhaponticin (Rhaponiticin,3',5-dihydroxy-4'-methoxystilbene 3- O-beta- D-glucopyranoside) from extracts of rhubarb rhizomes. These compounds showed significant hypoglycemic effects in streptozotocin (STZ)-induced type 1 diabetic rats and mice. In this study, we investigated the effect of rhaponticin(Rhaponiticin) on glucose utilization, lipid metabolism, and liver and heart function in a KK/Ay type 2 diabetic mouse model. The results showed that oral administration of rhaponticin (Rhaponiticin,125 mg/kg) significantly reduced blood glucose levels and improved oral glucose tolerance of KK/Ay diabetic mice. Elevated plasma triglyceride (TG), low density lipoprotein (LDL), cholesterol (CHO), non-esterified free fatty acids (NEFA), and insulin levels were also markedly attenuated. Serum enzymatic activities of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in the rhaponticin-treated group significantly decreased in comparison to the untreated model group. Livers of rhaponticin-treated mice had relatively normal cellular size and decreased fibrosis and steatosis. In addition, rhaponticin(Rhaponiticin) administration caused a remarkable increase in the hepatic glycogen content and a significant reduction in the hepatic triglyceride content. These results indicate that rhaponticin(Rhaponiticin) has a noticeable antidiabetic effect and could be potentially used as a new agent to treat type 2 diabetes mellitus and its complications.