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Kakkalide

$896

  • Brand : BIOFRON

  • Catalogue Number : BD-P0985

  • Specification : 98.5%(HPLC)

  • CAS number : 58274-56-9

  • Formula : C28H32O15

  • Molecular Weight : 608.549

  • PUBCHEM ID : 5490351

  • Volume : 25mg

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Catalogue Number

BD-P0985

Analysis Method

HPLC,NMR,MS

Specification

98.5%(HPLC)

Storage

2-8°C

Molecular Weight

608.549

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC=C(C=C1)C2=COC3=CC(=C(C(=C3C2=O)O)OC)OC4C(C(C(C(O4)COC5C(C(C(CO5)O)O)O)O)O)O

Synonyms

5-Hydroxy-6-methoxy-3-(4-methoxyphenyl)-4-oxo-4H-chromen-7-yl 6-O-β-D-xylopyranosyl-β-D-glucopyranoside/4H-1-Benzopyran-4-one, 5-hydroxy-6-methoxy-3-(4-methoxyphenyl)-7-[(6-O-β-D-xylopyranosyl-β-D-glucopyranosyl)oxy]-

IUPAC Name

5-hydroxy-6-methoxy-3-(4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxymethyl]oxan-2-yl]oxychromen-4-one

Applications

Kakkalide is an isoflavone derived from the flowers of Pueraria lobata. Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species (ROS)-associated inflammation[1].

Density

1.6±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

296.9±27.8 °C

Boiling Point

902.0±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C28H32O15/c1-37-12-5-3-11(4-6-12)13-8-39-15-7-16(26(38-2)22(33)18(15)19(13)30)42-28-25(36)23(34)21(32)17(43-28)10-41-27-24(35)20(31)14(29)9-40-27/h3-8,14,17,20-21,23-25,27-29,31-36H,9-10H2,1-2H3/t14-,17-,20+,21-,23+,24-,25-,27+,28-/m1/s1

InChl Key

QTVAYNGFFDZGDR-CIJVEFAYSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:58274-56-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

23190749

Abstract

Background: Kakkalide is the predominant isoflavone derived from the flowers of Pueraria lobata (Willd.) Ohwi. The aim of the present study was to investigate the effects of kakkalide on insulin resistance in the endothelium.
Methods: Human umbilical vein endothelial cells (HUVEC) were stimulated with 100 μmol/L palmitate (PA) for 30 min and the effects of 30 min pretreatment with 0.1-10 μmol/L kakkalide on reactive oxygen species (ROS)-associated inflammation in cells were evaluated by western blot analysis and reverse transcription-polymerase chain reaction. Furthermore, we investigated the biomodulation of insulin signaling by kakkalide along the insulin receptor substrate (IRS)-1/Akt/endothelial nitric oxide synthase (eNOS) pathway. We also determined the effects of 30 min pretreatment with 0.1-10 μmol/L kakkalide on insulin-mediated endothelium-dependent vasodilation of rat aorta in vitro following stimulation with 100 μmol/L PA.
Results: Kakkalide inhibited ROS overproduction and effectively restored mitochondrial membrane potential, demonstrating its chemoprotection of mitochondrial function. In addition, kakkalide inhibited ROS-associated inflammation in the endothelium by inhibiting tumor necrosis factor-α and interleukin-6 production and gene expression, as well as suppressing the phosphorylation of c-Jun N-terminal kinase and IκB kinase β/nuclear factor-κB. Inflammation impaired insulin phosphatidylinositol 3-kinase (PI3K) signaling and reduced insulin-mediated NO production in endothelial cells. Kakkalide facilitated PI3K signaling by positively regulating serine/tyrosine phosphorylation of IRS-1.
Conclusions: Kakkalide inhibited ROS-associated inflammation and ameliorated insulin-resistant endothelial dysfunction by beneficial effects on IRS-1 function.
© 2012 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd.

Title

Kakkalide Ameliorates Endothelial Insulin Resistance by Suppressing Reactive Oxygen Species-Associated Inflammation

Author

Dongyan Zhang 1 , Xuejiao Gao, Qi Wang, Minjian Qin, Kang Liu, Fang Huang, Baolin Liu

Publish date

2013 Mar

PMID

20686830

Abstract

The anti-inflammatory activities of kakkalide, a major constituent of the flower of Pueraria thunbergiana, and irisolidone, a metabolite of kakkalide produced by intestinal microflora, against carrageenan-induced inflammation in air pouches on the backs of mice and in lipopolysaccharide (LPS)-stimulated peritoneal macrophages were investigated. Kakkalide and irisolidone down-regulated the gene expression of cytokines [tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β)] and cyclooxygenase-2 (COX-2) and the production of pro-inflammatory cytokines, TNF-α and IL-1β, and inflammatory mediators, NO and prostaglandin E(2) (PGE(2)), in LPS-stimulated peritoneal macrophages. These agents also inhibited the phosphorylation of IκB-α and the nuclear translocation of nuclear factor-kappa B (NF-κB). Orally administered kakkalide and irisolidone significantly reduced carrageenan-induced inflammatory markers, leukocyte number, and protein amount in the exudates of the air pouch. These constituents also inhibited PGE(2) production and COX-2 inducible nitric oxide synthase, IL-1β, and TNF-α expression. These agents also inhibited NF-κB activation. The anti-inflammatory effects of irisolidone were more potent than those of kakkalide. Based on these findings, kakkalide and irisolidone may inhibit inflammatory reactions via NF-κB pathway, and irisolidone, a metabolite of kakkalide, may more potently inhibit these inflammatory reactions.

Title

Kakkalide and Its Metabolite Irisolidone Ameliorate Carrageenan-Induced Inflammation in Mice by Inhibiting NF-κB Pathway

Author

Sung-Won Min 1 , Young-Jun Park, Dong-Hyun Kim

Publish date

2011 Oct

PMID

31112869

Abstract

The flower of Pueraria lobata (family Fabaceae) has been clinically used in traditional Chinese medicine to counteract symptoms associated with drinking alcohol and liver injury and to alleviate inflammatory diseases. Its major constituent kakkalide is metabolized to irisolidone by gut microbiota. This research study was undertaken to understand the anti-colitis mechanism of kakkalide and irisolidone in vitro and in vivo. Kakkalide and its metabolite irisolidone inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation and TNF-α expression in macrophages. They also inhibited LPS-induced phosphorylation of IRAK1 and TAK1 and activation of NF-κB by inhibiting the binding of Alexa Fluor 488-conjugated LPS in vitro. Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Their treatments also protected epithelial cell disruption and infiltration of CD11b+/CD11c+ cells in the colon. Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-α, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. They also suppressed the fecal Proteobacteria population. Overall, the anti-colitic effects of irisolidone were superior to those of kakkalide. Kakkalide and its metabolite irisolidone inhibited inflammation in vitro and in vivo by inhibiting LPS binding to toll-like receptor 4 and gut proteobacteria population.

KEYWORDS

Colitis; Gut microbiota; Irisolidone; Kakkalide; Macrophages; Pueraria lobata.

Title

Kakkalide and Irisolidone Alleviate 2,4,6-trinitrobenzenesulfonic Acid-Induced Colitis in Mice by Inhibiting Lipopolysaccharide Binding to Toll-Like receptor-4 and Proteobacteria Population

Author

Hyo-Min Jang 1 , Keon-Tae Park 2 , Hyun-Deok Noh 2 , So-Hyeon Lee 2 , Dong-Hyun Kim 3

Publish date

2019 Aug