White crystalline powder
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
565.5ºC at 760mmHg
192 ºC (methanol )
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:2345-17-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
This study was designed to determine whether irisolidone and its glycoside kakkalide, which are the major constituents of the flower of Pueraria lobata (Kudzu) can attenuate ethanol-induced gastritic injury in mice.
METHODS AND RESULTS:
Irisolidone and kakkalide inhibited IL-8 secretion and NF-κB activation in lipopolysaccharide-stimulated KATO III cells. Therefore, we investigated their protective effects against ethanol-induced gastric injury in mice. Pretreatment with kakkalide or irisolidone decreased the area of hemorrhagic ulcerative lesions caused by ethanol and suppressed stomach myeloperoxidase activity, CXCL4 secretion, and NF-κB activation. The ameliorating effect of irisolidone was more potent than that of kakkalide.
Irisolidone may attenuate ethanol-induced gastritis by inhibiting the infiltration of immune cells, particularly neutrophils, through the regulation of CXCL-4 or IL-8 secretion.
© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Ethanol; Gastritis; Irisolidone; Kudzu; Neutrophil
Irisolidone attenuates ethanol-induced gastric injury in mice by inhibiting the infiltration of neutrophils.
Kang GD1, Lee SY1, Jang SE2, Han MJ2, Kim DH1.
2017 Feb 20
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.
Copyright © 2019 Elsevier B.V. All rights reserved.
Colitis; Gut microbiota; Irisolidone; Kakkalide; Macrophages; Pueraria lobata
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.
Jang HM1, Park KT2, Noh HD2, Lee SH2, Kim DH3.
Irisolidone, a major isoflavone found in Pueraria lobata flowers, exhibits a wide spectrum of bioactivities, while its metabolic pathways and the pharmacokinetics of its metabolites in vivo have not been investigated yet. In the present study, an ultra performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UHPLC/Q-TOF MS) method was employed to investigate the metabolic pathways of irisolidone and the pharmacokinetics of its main metabolites in rats, after a single 100mg/kg oral dose of irisolidone. Protein precipitation method was used to prepare plasma samples. A total of 15 metabolites included irisolidone were detected and tentatively identified based on the mass spectral fragmentation patterns, elution order or confirmed using available reference standards. The pharmacokinetics of the main metabolites included three glucuronide metabolites tectorigenin-7-O-glucuronide (Te-7G), 6-hydroxybiochanin A-6-O-glucuronide (6-OH-BiA-6G), irisolidone-7-O-glucuronide (Ir-7G), and three sulfate metabolite tectorigenin-7-O-sulfate-4′-O-sulfate (Te-7S-4’S), tectorigenin-7-O-sulfate (Te-7S) and irisolidone-7-O-sulfate (Ir-7S), and aglycone tectorigenin (Te), and irisolidone (Ir) were evaluated. The plasma concentrations reached maximal values of 0.297μmol/L at 10.3h for Te-7S-4’S, 0.199μmol/L at 21.7h for Te-7G, 0.154μmol/L at 8.00h for Te-7S, 4.10μmol/L at 15.3h for 6-OH-BiA-6G, 10.7μmol/L at 9.71h for Ir-7G, 0.918μmol/L at 11.3h for Te, 0.150μmol/L at 8.67h for Ir-7S, and 0.843μmol/L at 9.67h for Ir, respectively. Since the total plasma concentrations of conjugated metabolites were much higher than that of the irisolidone aglycone, an extensive phase II metabolism plays an important role in the pharmacokinetics of irisolidone in vivo.
Copyright © 2015 Elsevier B.V. All rights reserved.
Irisolidone; Metabolites; Plasma pharmacokinetics; Rat; UHPLC/Q-TOF MS
Pharmacokinetics of irisolidone and its main metabolites in rat plasma determined by ultra performance liquid chromatography/quadrupole time-of-flight mass spectrometry.
Zhang G1, Qi W2, Xu L2, Kano Y2, Yuan D3.
2015 Nov 15