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Peiminine

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-P3008

  • Specification : 98%

  • CAS number : 18059-10-4

  • Formula : C27H43NO3

  • Molecular Weight : 429.64

  • PUBCHEM ID : 167691

  • Volume : 25mg

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Catalogue Number

BF-P3008

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

429.64

Appearance

White crystalline powder

Botanical Source

Fritillaria thunbergii

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC2C(C3CCC4C(C3CN2C1)CC5C4CC(=O)C6C5(CCC(C6)O)C)(C)O

Synonyms

(3β)-3,20-Dihydroxycevan-6-one/Osnovanine/Raddeamine/(3β,5α)-3,20-Dihydroxycevan-6-one/Cevan-6-one, 3,20-dihydroxy-, (3β,5α)-/Sipeimine/3beta,20-Dihydroxy-5alpha-cevan-6-one/3β,20-Dihydroxy-5α-cevan-6-one/(3b)-3,20-Dihydroxycevan-6-one/RADDEANINE/Cevan-6-one, 3,20-dihydroxy-, (3β)-/cevan-6-one, 3,20-dihydroxy-, (3b)-/PEINININE/Fritillarine/Verticinone

IUPAC Name

(1R,2S,6S,9S,10S,11S,14S,15S,18S,20S,23R,24S)-10,20-dihydroxy-6,10,23-trimethyl-4-azahexacyclo[12.11.0.02,11.04,9.015,24.018,23]pentacosan-17-one

Density

1.2±0.1 g/cm3

Solubility

Methanol

Flash Point

296.8±30.1 °C

Boiling Point

567.1±50.0 °C at 760 mmHg

Melting Point

212-213ºC

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2942000000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:18059-10-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29534526

Abstract

Neuroinflammation, characterized marked by microglial activation, plays a very important role in the pathogenesis of Parkinson’s disease (PD). Upon activation, pro-inflammatory mediators are produced by microglia, triggering excessive inflammatory responses and ultimately damaging dopaminergic neurons. Therefore, the identification of agents that inhibit neuroinflammation may be an effective approach for developing novel treatments for PD. In this study, we sought to investigate whether peiminine protects dopaminergic neurons by inhibiting neuroinflammation. We evaluated the effects of peiminine on behavioural dysfunction, microglial activation and the loss of dopaminergic neurons in a rat model of lipopolysaccharide (LPS)-induced PD. BV-2 cells were pretreated with peiminine for 1 h and then stimulated with LPS for different times. Then, inflammatory responses and the related signalling pathways were analysed. Peiminine markedly attenuated behavioural dysfunction and inhibited the loss of dopaminergic neurons and microglial activation in the LPS-induced PD rat model. In BV-2 cells, peiminine significantly decreased LPS-induced expression of the pro-inflammatory mediators TNF-α, IL-6 and IL-1β, COX-2 and iNOS by inhibiting the phosphorylation of ERK1/2, AKT and NF-κB p65. Based on these results demonstrated that peiminine has a role in protecting dopaminergic neurons in the LPS-induced PD rat model by inhibiting neuroinflammation.

KEYWORDS

AKT; ERK1/2; NF-κB; Parkinson’s disease; microglia; peiminine.

Title

Peiminine Protects Dopaminergic Neurons From Inflammation-Induced Cell Death by Inhibiting the ERK1/2 and NF-κB Signalling Pathways

Author

Guangxin Chen 1 , Juxiong Liu 2 , Liqiang Jiang 3 , Xin Ran 4 , Dewei He 5 , Yuhang Li 6 , Bingxu Huang 7 , Wei Wang 8 , Dianfeng Liu 9 , Shoupeng Fu 10

Publish date

2018 Mar 12

PMID

28496003

Abstract

Peiminine, a compound extracted from the bulbs of Fritillaria thunbergii and traditionally used as a medication in China and other Asian countries, was reported to inhibit colorectal cancer cell proliferation and tumor growth by inducing autophagic cell death. However, its mechanism of anticancer action is not well understood, especially at the metabolic level, which was thought to primarily account for peiminine’s efficacy against cancer. Using an established metabolomic profiling platform combining ultra-performance liquid chromatography/tandem mass spectrometry with gas chromatography/mass spectrometry, we identified metabolic alterations in colorectal cancer cell line HCT-116 after peiminine treatment. Among the identified 236 metabolites, the levels of 57 of them were significantly (p < 0.05) different between peiminine-treated and -untreated cells in which 45 metabolites were increased and the other 12 metabolites were decreased. Several of the affected metabolites, including glucose, glutamine, oleate (18:1n9), and lignocerate (24:0), may be involved in regulation of the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin (mTOR) pathway and in the oxidative stress response upon peiminine exposure. Peiminine predominantly modulated the pathways responsible for metabolism of amino acids, carbohydrates, and lipids. Collectively, these results provide new insights into the mechanisms by which peiminine modulates metabolic pathways to inhibit colorectal cancer cell growth, supporting further exploration of peiminine as a potential new strategy for treating colorectal cancer.

KEYWORDS

AKT; ERK1/2; NF-κB; Parkinson’s disease; microglia; peiminine.

Title

Peiminine Inhibits Colorectal Cancer Cell Proliferation by Inducing Apoptosis and Autophagy and Modulating Key Metabolic Pathways

Author

Zhi Zheng 1 2 3 , Liting Xu 1 2 , Shuofeng Zhang 4 , Wuping Li 1 , Fangfang Tou 1 2 , Qinsi He 1 2 , Jun Rao 1 2 , Qiang Shen 3

Publish date

2017 Jul 18

PMID

30200569

Abstract

Peiminine, an alkaloid extracted from Fritillaria plants, has been reported to have potent anti-inflammatory properties. However, the anti-inflammatory effect of peiminine on a mouse lipopolysaccharide (LPS)-induced mastitis model remains to be elucidated. The purpose of this experiment was to investigate the effect of peiminine on LPS-induced mastitis in mice. LPS was injected through the canals of the mammary gland to generate the mouse LPS-induced mastitis model. Peiminine was administered intraperitoneally 1 h before and 12 h after the LPS injection. In vitro, mouse mammary epithelial cells (mMECs) were pretreated with different concentrations of peiminine for 1 h and were then stimulated with LPS. The mechanism of peiminine on mastitis was studied by hematoxylin-eosin staining (H&E) staining, western blotting, and enzyme-linked immunosorbent assay (ELISA). The results showed that peiminine significantly decreased the histopathological impairment of the mammary gland in vivo and reduced the production of pro-inflammatory mediators in vivo and in vitro. Furthermore, peiminine inhibited the phosphorylation of the protein kinase B (AKT)/ nuclear factor-κB (NF-κB), extracellular regulated protein kinase (ERK1/2), and p38 signaling pathways both in vivo and in vitro. All the results suggested that peiminine exerted potent anti-inflammatory effects on LPS-induced mastitis in mice. Therefore, peiminine might be a potential therapeutic agent for mastitis.

KEYWORDS

AKT/NF-κB; ERK1/2; LPS; mastitis; p38; peiminine.

Title

Peiminine Protects Against Lipopolysaccharide-Induced Mastitis by Inhibiting the AKT/NF-κB, ERK1/2 and p38 Signaling Pathways

Author

Qian Gong 1 , Yanwei Li 2 , He Ma 3 , Wenjin Guo 4 , Xingchi Kan 5 , Dianwen Xu 6 , Juxiong Liu 7 , Shoupeng Fu 8

Publish date

2018 Sep 6


Description :

Peiminine(Verticinone; Raddeanine) is a natural compound with anti-inflammatory activity.IC50 value:Target:Peiminine and DXS significantly reduced alveolar inflammation and pulmonary interstitial inflammation in rats with bleomycin-induced lung injury. peiminine inhibits lung inflammation and pulmonary fibrosis in a rat model of bleomycin-induced lung injury, by reducing circulating IFN-γ levels and inhibiting signal transduction pathways involving TGF-β, CTGF, ERK1/2, NF-κB and FasL.