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Oxymatrine

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-O1004

  • Specification : 98%

  • CAS number : 16837-52-8

  • Formula : C15H24N2O2

  • Molecular Weight : 264.36

  • PUBCHEM ID : 114850

  • Volume : 20mg

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Catalogue Number

BF-O1004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

264.36

Appearance

Colorless lump crystal

Botanical Source

Sophora flavescens,Sophora alopecuroides,Euchresta japonica

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C1CC2C3CCC[N+]4(C3C(CCC4)CN2C(=O)C1)[O-]

Synonyms

(7aS,13aR,13bR,13cS)-dodecahydro-1H,5H,10H-dipyrido[2,1-f:3’,2’,1’-ij][1,6]naphthyridin-10-one 4-oxide/(4R,7aS,13aR,13bR,13cS)-dodecahydro-1H,5H,10H-dipyrido[2,1-f:3’,2’,1’-ij][1,6]naphthyridin-10-one 4-oxide/Ammothamnine/Matrine N-oxide/(7aS,13aR,13bR,13cS)Dodecahydro-1H,5H,10H-dipyrido[2,1-f:3',2',1'-ij][1,6]naphthyridin-10-one 4-oxide/1H,5H,10H-Dipyrido[2,1-f:3',2',1'-ij][1,6]naphthyridin-10-one, dodecahydro-, 4-oxide, (7aS,13aR,13bR,13cS)-/Oxymatrine

IUPAC Name

(1R,2R,9S,17S)-13-oxido-7-aza-13-azoniatetracyclo[7.7.1.02,7.013,17]heptadecan-6-one

Density

Solubility

Methanol; Chloroform; Water

Flash Point

Boiling Point

Melting Point

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#:16837-52-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29241159

Abstract

The fibroblast-like synoviocytes (FLSs) has the aggressive phenotype, which is very important for cartilage destruction in rheumatoid arthritis (RA). To the pathology of RA, the increased FLSs migration, activation and proliferation are essential factors. Oxymatrine is a traditional Chinese herb, which is the extraction from the root of Sophora flavescens and regarded as quinolizidine alkaloid compounds and has been shown to inhibit inflammation, proliferation and migration in vitro or vivo. However, whether oxymatrine effects in the treatment of RA FLSs is undefined. In our study, the inhibition of oxymatrine in RA FLSs inflammation, proliferation and migration in RA FLS are evaluated. We found that oxymatrine decreased the IL-6 and IL-8 expression and the proliferation, migration and invasion of RA FLSs. We also evaluated the molecular mechanisms and we found the effect of oxymatrine on NF-κB activation. The results showed that oxymatrine inhibited the activity of NF-κB. And the treatment activity of oxymatrine on collagen-induced arthritis (CIA) was further explored by us. Thus, we conclude that oxymatrine may protect joint destruction of RA by inhibiting synoviocyte activation, migration, invasion, and proliferation.

KEYWORDS

Fibroblast-like synoviocytes; Inflammation; Migration; NF-κB; Oxymatrine.

Title

Oxymatrine Prevents Synovial Inflammation and Migration via Blocking NF-κB Activation in Rheumatoid Fibroblast-Like Synoviocytes

Author

Jiang Liang 1 , Boyang Chang 2 , Mingcheng Huang 3 , Weichen Huang 4 , Wukai Ma 5 , Yang Liu 5 , Wan Tai 5 , Yi Long 5 , Yun Lu 5

Publish date

2018 Feb 14;

PMID

29328383

Abstract

Previous studies have demonstrated that oxymatrine may inhibit ventricular remodeling and serves an important role in the treatment of cardiovascular disease. The present study investigated whether oxymatrine treatment protects against the effects of cardiopulmonary resuscitation (CPR) via regulation of the transforming growth factor‑β1 (TGF‑β1)/mothers against decapentaplegic (Smad) signaling pathway. A CPR model was established in Sprague‑Dawley (SD) rats by asphyxiation, and rats were subsequently anaesthetized by intraperitoneal injection of chloral hydrate. SD rats were then administered 25 or 50 mg/kg oxymatrine once a day for 4 weeks. Oxymatrine treatment significantly improved troponin I levels, the ejection fraction, hydroxyproline content and the myocardial performance index in model rats. However, treatment with oxymatrine significantly reduced arterial oxygen tension, arterial lactate levels and oxygen extraction. Treatment with oxymatrine following CPR significantly inhibited the protein expression levels of TGF‑β1, TGF‑β1 receptor type 1 and Smad homolog 3 (Smad3) in model rats. The results of this research indicated that oxymatrine treatment may protect against the effects of CPR via regulation of the TGF‑β1/Smad3 signaling pathway and may be a novel drug for CPR in a clinical setting.

KEYWORDS

Fibroblast-like synoviocytes; Inflammation; Migration; NF-κB; Oxymatrine.

Title

Oxymatrine Protects Against the Effects of Cardiopulmonary Resuscitation via Modulation of the TGF-β1/Smad3 Signaling Pathway

Author

Dawei Wang 1 , Xiao Qian Lou 2 , Xiao-Ming Jiang 1 , Chenxi Yang 3 , Xiao-Liang Liu 1 , Nan Zhang 1

Publish date

2018 Mar

PMID

28946137

Abstract

Background/aims: Doxorubicin-induced cardiac toxicity has been a major concern of oncologists and is considered the main restriction on its clinical application. Oxymatrine has shown potent anti-cancer, anti-fibrosis, and anti-oxidative effects. Recently, it has been reported that oxymatrine is protective against some cardiovascular diseases. In this study, we aimed to investigate the effects of oxymatrine on doxorubicin-induced cardiotoxicity in rat hearts and H9c2 cells.
Methods: Creatine Kinase – MB (CK-MB) and Lactate Dehydrogenase (LDH) levels were determined using commercial kits. Biochemical indices reflecting oxidative stress, such as catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were also analyzed with commercial kits. Mitochondrial reactive oxygen species (ROS) 2′,7′-dichlorofluorescin diacetate (DCFH-DA) was measured by fluorescence microscopy. Histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. Western blots were used to detect the level of expression of cleaved caspase-3.
Results: Doxorubicin treatment significantly increased oxidative stress levels, as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen species. Doxorubicin also increased pathological damage in myocardial tissue, myocardial ROS levels, and malonyldialdehyde levels, and induced apoptosis in myocardial tissues and H9c2 cells. All of these doxorubicin-induced effects were attenuated by oxymatrine.
Conclusion: These in vitro and in vivo findings indicate that oxymatrine may be a promising cardioprotective agent against doxorubicin-induced cardiotoxicity, at least in part mediated through oxymatrine’s inhibition of cardiac apoptosis and oxidative stress.

KEYWORDS

Apoptosis; Cardiotoxicity; Doxorubicin; Oxidative stress; Oxymatrine.

Title

Oxymatrine Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats

Author

Yan-Yan Zhang 1 , Minhan Yi 2 3 , Yong-Pan Huang 1

Publish date

2017


Description :

Oxymatrine, an alkaloid from the roots of Sophora species, with anti-inflammatory, antifibrosis, and antitumor effects, inhibits the iNOS expression and TGF-β/Smad pathway.